Disease |
Disease |
Method |
Sample |
Expression pattern |
Dysfunction type |
Description |
PMID |
Source |
paraspeckle disintegration |
Immunoprecipitation of Ribonucleoprotein Complex,knockdown |
HeLa cell |
down-regulated |
mutation |
Successful removal of MENepsilon/beta by a refined knockdown method resulted in paraspeckle disintegration. Furthermore, the reassembly of paraspeckles disassembled by transcriptional arrest appeared to be unsuccessful in the absence of MENepsilon/beta. |
19188602 |
|
lung cancer |
knockdown |
human bronchial epithelial (HBE) cells |
up-regulated |
interaction |
Cigarette smoke extract (CSE) caused decreases of miR-217 levels and increases in lncRNA MALAT1 levels. The CSE-induced increase of MALAT1 expression was blocked by an miR-217 mimic, indicating that miR-217 negatively regulates MALAT1 expression. |
26415832 |
|
breast cancer |
MALAT1-siRNA |
breast cancer tissues and cells |
up-regulated |
N/A |
MALAT1-siRNA inhibited breast cancer cell proliferation and cell cycle progression in vitro and in vivo; and downregulating miR-124 expression |
26918449 |
|
non-small cell lung cancer |
Meta-analysis |
non-small cell lung cancer and pancreatic cancer |
up-regulated |
expression |
From subgroup analyses,we present evidence that lncRNA MALAT1 overexpression was an unfavorable prognostic factor for patients' overall survival in non-small cell lung cancer and pancreatic cancer, the pooled HRs (95% CI) were 1.86 (95% CI 1.27-2.73) and 1.78 (95% CI 1.30-2.44), respectively. In conclusion, lncRNA MALAT1 is a potential prognostic factor in human cancers. |
26131129 |
|
pancreatic cancer |
Meta-analysis |
non-small cell lung cancer and pancreatic cancer |
up-regulated |
expression |
From subgroup analyses,we present evidence that lncRNA MALAT1 overexpression was an unfavorable prognostic factor for patients' overall survival in non-small cell lung cancer and pancreatic cancer, the pooled HRs (95% CI) were 1.86 (95% CI 1.27-2.73) and 1.78 (95% CI 1.30-2.44), respectively. In conclusion, lncRNA MALAT1 is a potential prognostic factor in human cancers. |
26131129 |
|
cervical cancer |
Microarray, knockdown, RT-PCR, western blot, and immunofluorescence |
cervical cancer (CC) cells and tissues |
up-regulated |
expression |
The down-regulation of MALAT1 by shRNA in CC cells inhibited the invasion and metastasis in vitro and in vivo. MALAT1 functions to promote cervical cancer invasion and metastasis via induction of EMT, and it may be a target for the prevention and therapy of cervical cancers. |
26798987 |
|
neuroblastoma |
microarray, qPCR etc. |
cell line (SK-N-SH ) |
down-regulated |
expression |
We identified a shorter transcriptional initiation site and found that CREB binds to the defined proximal promoter of the MALAT1 gene. The expression of the tumor marker MALAT1 ncRNA is sensitive to cell surface receptor activation by oxytocin in a neuroblastoma cell line. |
20149803 |
LncRNADisease Lnc2Cancer
|
ovarian cancer |
microarray, qPCR etc. |
ovarian cancer tissue, cell lines (SKOV3, SKOV3.ip1 etc.) |
down-regulated |
N/A |
The qPCR results of seven lncRNAs (MALAT1, H19, UCA1, CCAT1, LOC645249, LOC100128881, and LOC100292680) were consistent with the deregulation found by microarray analysis, reflecting the reliability of the microarray data to some extent. |
24379988 |
Lnc2Cancer
|
triple-negative breast cancer |
microarray, qPCR etc. |
triple-negative breast cancer tissue |
up-regulated |
expression |
We found that the expression levels of TCONS_l2_00003938, ENST00000460164, ENST00000425295, MALAT1 and HOTAIR were significantly higher in tumor tissues than non-tumor tissues, whereas there were no significant differences in the expression levels of the other 3 lncRNAs. Our study identified a set of lncRNAs that were consistently aberrantly expressed in TNBC, and these dysregulated lncRNAs may be involved in the development and/or progression of TNBC. |
25996380 |
Lnc2Cancer
|
papillary thyroid carcinoma |
microarray, qPCR etc. |
papillary thyroid carcinoma tissue |
down-regulated |
expression |
Expression profiles of five lnc-RNAs (MEG3, HULC, HOTAIR, NEAT1, and MALAT-1) previously shown to be involved in cancer metastasis were detected by qPCR in 5 pairs of papillary thyroid cancer and 11 matched lymph node metastatic tissues. Among the five, MEG3 showed significant down-expression. Overexpression of MEG3 inhibits thyroid cancer cell migration and invasion. |
25997963 |
Lnc2Cancer
|
neuroblastoma |
microarray, qPCR, knockdown etc. |
cell lines (BE(2)-C, CHP134) |
up-regulated |
N/A |
Here we demonstrated that N-Myc up-regulated the expression of JMJD1A in N-Myc oncogene-amplified human neuroblastoma cells by directly binding to the JMJD1A gene promoter. Affymetrix microarray studies revealed that the gene second most significantly up-regulated by JMJD1A was MALAT1. Consistent with this finding, RT-PCR and chromatin immunoprecipitation assays showed that JMJD1A bound to the MALAT1 gene promoter and demethylated histone H3K9 at the MALAT1 gene promoter. |
24742640 |
Lnc2Cancer
|
colon cancer |
microarray, qPCR, knockdown etc. |
blood, cell lines (SW480 and SW620) |
up-regulated |
regulation |
The stimulation of colon cancer progression by TADC-derived CCL5 was associated with the up-regulation of non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT-1), which subsequently increased the expression of Snail. Blocking MALAT-1 significantly decreased the TADC-conditioned medium and CCL5-mediated migration and invasion by decreasing the enhancement of Snail, suggesting that the MALAT-1/Snail pathway plays a critical role in TADC-mediated cancer progression |
25546229 |
Lnc2Cancer
|
colorectal cancer |
microarray, qPCR, Western blot etc. |
CRC tissue, cell lines (HCT116, SW480, SW620, LoVo, CaCo-2 etc.) |
up-regulated |
regulation |
In the present study, we found that MALAT1 was up-regulated in human primary CRC tissues with lymph node metastasis. Knockdown of MALAT1 inhibited CRC tumor growth and metastasis. MALAT1 regulated at least 243 genes in CRC cells in a genome-wide expression profiling. Among these genes, PRKA kinase anchor protein 9 (AKAP-9) was significantly up-regulated at both mRNA and protein levels. AKAP-9 was highly expressed in CRC cells with metastatic potential and human primary CRC tissues with lymph node metastasis. |
25446987 |
Lnc2Cancer
|
glioma |
microarray, qPCR, Western blot, knockdown etc. |
cell line SHG139S |
down-regulated |
interaction |
Our results showed that downregulation of MALAT1 suppressed the expression of Sox2 and Nestin which are related to stemness, while downregulation of MALAT1 promoted the proliferation in SHG139S. Further research on the underlying mechanism showed that the effects of MALAT1 downregulation on SHG139S were through regulating ERK/MAPk signaling activity. And we also found that downregulation of MALAT1 could activate ERK/MAPK signaling and promoted proliferation in SHG139 cells. |
26649728 |
Lnc2Cancer
|
liver cancer |
microarray, qPCR, Western blot, Luciferase reporter assay, RIP etc. |
liver cancer tissue, cell lines (HepG2, Bel-7402, SMMC-7721, HEK-293T etc.) |
differential expression |
regulation |
Mutual inhibition between YAP and SRSF1 maintains long non-coding RNA, Malat1-induced tumourigenesis in liver cancer. |
24468535 |
LncRNADisease Lnc2Cancer
|
proliferative vitreoretinopathy |
Microarray, qRT-PCR |
biofluid of PVR (Proliferative VitreoRetinopathy) patients |
up-regulated |
expression |
MALAT1 was significantly up-regulated in the cellular and plasma fraction of peripheral blood in PVR patients. In vitro experiments revealed the role of MALAT1 in regulating RPE proliferation and migration, which is critical for ERMs formation. MALAT1 is a potential prognostic indicator and a target for the diagnosis and gene therapy for PVR diseases. |
26241674 |
|
non-small-cell lung cancer |
microarray, qRT-PCR |
tumor samples from 383 NSCLC patients |
N/A |
interaction |
Gene expression analysis of A549 adenocarcinoma cells with differential MALAT-1 lncRNA expression demonstrated an influence on the expression of Bcl-2 and its interacting proteins. |
25036876 |
|
non-small cell lung cancer |
N/A |
N/A |
N/A |
expression |
In NSCLC metastasizing tumors, MALAT-1 expression is three-fold higher than in non-metastasizing tumors. Furthermore, in patients with stage I disease, MALAT-1 expression is closely correlated with poor prognosis. |
21550244 |
LncRNADisease
|
hepatocellular carcinoma |
N/A |
hepatocellular carcinoma (HCC) tissues |
up-regulated |
interaction |
N/A |
26352013 |
|
breast cancer |
N/A |
breast cancer cells |
up-regulated |
N/A |
MALAT1 induced migration and invasion of breast cancer |
26926567 |
|
hepatocelluar carcinoma |
N/A |
N/A |
N/A |
expression |
HCC and HPBL have clearly different patterns of gene expression, with genes IGF2, Fibronectin, DLK1, TGFb1, MALAT1 and MIG6 being over-expressed in HPBL versus HCC |
17006932 |
LncRNADisease
|
lung adenocarcinoma |
N/A |
N/A |
N/A |
expression |
Metastasis associated lung adenocarcinoma transcript 1 is up-regulated in placenta previa increta/percreta and strongly associated with trophoblast-like cell invasion in vitro. |
19690017 |
LncRNADisease
|
cancer |
N/A |
N/A |
N/A |
expression |
The expression of the long ncRNA MALAT1 correlates with tumor development, progression or survival in lung, liver and breast cancer. |
20711585 |
LncRNADisease
|
cancer |
N/A |
N/A |
N/A |
expression |
MALAT1 is a highly conserved long ncRNA originally identified as a transcript overexpressed in many cancers. |
20864030 |
LncRNADisease
|
osteosarcoma |
N/A |
N/A |
N/A |
expression |
Osteosarcoma patients' survival is significantly associated with MALAT-1 expression levels. |
20951849 |
LncRNADisease
|
non-small cell lung cancer |
N/A |
N/A |
N/A |
expression |
Specific lncRNAs can serve as predictors of tumor outcome, as shown with the expression of the lncRNA MALAT-1 in early-stage non-small cell lung cancer. |
21903344 |
LncRNADisease
|
breast cancer |
N/A |
N/A |
N/A |
regulation |
On a more mechanistic level, recent studies have revealed the contribution of lncRNAs as proto-oncogenes, e.g. GAGE6, as tumor suppressor genes, e.g. 鈥榩15 antisense RNA and lincP21' (36,91), as drivers of metastatic transformation, e.g. HOTAIR in breast cancer, and as regulators of alternative splicing, e.g. MALAT1 |
22492512 |
LncRNADisease
|
hepatocelluar carcinoma |
N/A |
N/A |
N/A |
mutation |
We conducted a case-control study and genotyped two SNPs, rs7763881 in HULC and rs619586 in MALAT1 Furthermore, the variant genotypes of rs619586 was associated with decreased HCC risk with a borderline significance. |
22493738 |
LncRNADisease Lnc2Cancer
|
non-small cell lung cancer |
N/A |
N/A |
N/A |
expression |
lncRNA-associated disruption to alternative splicing has also been reported in non-small cell lung cancer by virtue of overexpression of MALAT1 |
22817756 |
LncRNADisease
|
small cell lung cancer |
N/A |
N/A |
N/A |
expression |
For other LncRNAs, specific targets have yet to be identified. This is the case of MALAT1, a LncRNA whose expression is three times higher in metastasizing early-stage non-small cell lung cancer vs. non-metastasizing tumours |
22928560 |
LncRNADisease
|
breast cancer |
N/A |
N/A |
N/A |
regulation |
Sequesters SR splicing factors to regulate alternative splicing. |
22996375 |
LncRNADisease
|
colon cancer |
N/A |
N/A |
N/A |
regulation |
Sequesters SR splicing factors to regulate alternative splicing. |
22996375 |
LncRNADisease
|
liver cancer |
N/A |
N/A |
N/A |
regulation |
Sequesters SR splicing factors to regulate alternative splicing. |
22996375 |
LncRNADisease
|
lung cancer |
N/A |
N/A |
N/A |
regulation |
Sequesters SR splicing factors to regulate alternative splicing. |
22996375 |
LncRNADisease
|
osteosarcoma |
N/A |
N/A |
N/A |
regulation |
Sequesters SR splicing factors to regulate alternative splicing. |
22996375 |
LncRNADisease
|
pancreatic cancer |
N/A |
N/A |
N/A |
regulation |
Sequesters SR splicing factors to regulate alternative splicing. |
22996375 |
LncRNADisease
|
prostate cancer |
N/A |
N/A |
N/A |
regulation |
Sequesters SR splicing factors to regulate alternative splicing. |
22996375 |
LncRNADisease
|
uterus cancer |
N/A |
N/A |
N/A |
regulation |
Sequesters SR splicing factors to regulate alternative splicing. |
22996375 |
LncRNADisease
|
cancer |
N/A |
N/A |
N/A |
regulation |
MALAT1 (metastasis-associated lung adenocarcinoma transcript 1),another lncRNA associated with various cancers and metastasis (Ji et al. 2003; Lin et al. 2011)锛?, is found to affect the transcriptional and post-transcriptional regulation of cytoskeletal and extracellular matrix genes. |
23463798 |
LncRNADisease
|
decreased myogenesis |
N/A |
N/A |
N/A |
expression |
The myostatin-induced inhibition of the long noncoding RNA Malat1 is associated with decreased myogenesis. |
23485710 |
LncRNADisease
|
cancer |
N/A |
N/A |
N/A |
expression |
MALAT1 is upregulated in several cancer types and its overexpression has been linked to an increase in cell proliferation and migration in lung and colorectal cancer cells. |
23660942 |
LncRNADisease
|
bladder cancer |
N/A |
N/A |
N/A |
expression |
Theseguilty by association studies have found numerous bladder-cancer associated lncRNAs |
24006935 |
LncRNADisease
|
hepatocelluar carcinoma |
N/A |
N/A |
N/A |
expression |
Dysregulation and functional roles of lncRNAs in HCC |
24183851 |
LncRNADisease
|
bladder cancer |
N/A |
N/A |
N/A |
regulation |
Oncogene |
24373479 |
LncRNADisease
|
kidney cancer |
N/A |
N/A |
N/A |
regulation |
Oncogene |
24373479 |
LncRNADisease
|
prostate cancer |
N/A |
N/A |
N/A |
regulation |
Putative marker |
24373479 |
LncRNADisease
|
diabetes mellitus |
N/A |
N/A |
N/A |
expression |
In addition, MALAT1, a conserved lncRNA, was significantly upregulated in an RF/6A cell model of hyperglycemia, in the aqueous humor samples, and in fibrovascular membranes of diabetic patients. |
24436191 |
LncRNADisease
|
breast cancer |
N/A |
N/A |
N/A |
regulation |
invasion & metastasis pancreas, colon, prostate liver, cervix, neuroblastoma osteosarcoma |
24499465 |
LncRNADisease
|
lung cancer |
N/A |
N/A |
N/A |
regulation |
invasion & metastasis pancreas, colon, prostate liver, cervix, neuroblastoma osteosarcoma |
24499465 |
LncRNADisease
|
uterus cancer |
N/A |
N/A |
N/A |
regulation |
invasion & metastasis pancreas, colon, prostate liver, cervix, neuroblastoma osteosarcoma |
24499465 |
LncRNADisease
|
lung cancer |
N/A |
N/A |
N/A |
expression |
MALAT1, also known as NEAT2 (nuclear-enriched abundant transcript 2), was initially discovered as a predictive biomarker for metastasis development in lung cancer. |
24667321 |
LncRNADisease
|
tumor |
N/A |
N/A |
N/A |
regulation |
MALAT1 plays a role in cell migration and tumor metastasis, as demonstrated by knockout of MALAT1 in lung cancer cell lines (Gutschner et al., 2013). |
24721780 |
LncRNADisease
|
cancer |
N/A |
N/A |
N/A |
regulation |
They found that MALAT1 did not alter alternative splicing but rather actively regulated gene expression including a set of metastasis-associated genes. Consequently, MALAT1-deficient cells were impaired in migration and formed fewer tumor nodules in mouse xenograft. Antisense oligonucleotides (ASO) that block MALAT1 prevented metastasis formation after tumor implantation. |
24757675 |
LncRNADisease
|
cervical cancer |
N/A |
N/A |
N/A |
expression |
Overexpressed MALAT1 was found in many solid tumors such as lung cancer, cervical cancer, and HCC. |
24757675 |
LncRNADisease
|
hepatocelluar carcinoma |
N/A |
N/A |
N/A |
expression |
Overexpressed MALAT1 was found in many solid tumors such as lung cancer, cervical cancer, and HCC. |
24757675 |
LncRNADisease
|
lung cancer |
N/A |
N/A |
N/A |
expression |
Overexpressed MALAT1 was found in many solid tumors such as lung cancer, cervical cancer, and HCC. |
24757675 |
LncRNADisease
|
laryngeal squamous cell carcinoma |
N/A |
N/A |
N/A |
expression |
The result suggested that the MALAT1 was up-regulated in primary LSCC compared with adjacent non-cancerous tissues. |
24817925 |
LncRNADisease
|
nasopharyngeal carcinoma |
N/A |
N/A |
N/A |
expression |
The result found that MALAT1 was most highly expressed in 5-8F cells (high rate to be tumor and metastasis), and up-regulated in CNE-2, C666-1 and HONE-1 which is higher malignant and poorly differentiated nasopharyngeal squamous cell carcinoma, while least expressed in NP69 epithelial cells of the eternal life. The data indicated that MALAT1 might be related to the metastasis and differentiation of NPC cells. |
24817925 |
LncRNADisease
|
acute myocardial infarction |
N/A |
N/A |
N/A |
N/A |
Level of metastasis-associated lung adenocarcinoma transcript 1 was higher in patients with MI than in healthy volunteers (P<0.01); Patients with ST-segment-elevation MI had lower levels of metastasis-associated lung adenocarcinoma transcript 1 (P=0.005) when compared with patients with non-ST-segment-elevation |
25035150 |
LncRNADisease
|
diabetes mellitus |
N/A |
N/A |
N/A |
N/A |
MALAT1 expression is significantly upregulated in the retinas of STZ-induced diabetic rats and db/db mice. MALAT1 knockdown could obviously ameliorate DR in vivo, as shown by pericyte loss, capillary degeneration, microvascular leakage, and retinal inflammation. Moreover, MALAT1 knockdown could regulate retinal endothelial cell proliferation, migration, and tube formation in vitro. The crosstalk between MALAT1 and p38 MAPK signaling pathway is involved in the regulation of endothelial cell function. |
25356875 |
LncRNADisease
|
glioblastoma |
N/A |
N/A |
N/A |
N/A |
Extensive microRNA-mediated crosstalk between lncRNAs and mRNAs in mouse WIF1 re-expression in glioblastoma inhibits migration through attenuation of non-canonical WNT signaling by downregulating the lncRNA MALAT1. |
25772239 |
LncRNADisease
|
non-small cell lung cancer |
qPCR etc. |
NSCLC tissue |
up-regulated |
expression |
Increased expression of the lncRNA MALAT-1 has been observed in several types of tumors, including metastatic non-small cell lung cancer. |
12970751 |
LncRNADisease Lnc2Cancer
|
osteosarcoma |
qPCR etc. |
osteosarcoma tissue |
up-regulated |
N/A |
The expression of MALAT-1, IMPDH2, FTL and RHOA significantly correlated with response to chemotherapy. Expression of all four genes was increased in the poor responder group that are valuable markers for the prediction of osteosarcoma therapy outcome. Especially IMPDH2 and FTL are promising candidates for the stratification of osteosarcoma patients into low- and high-risk groups. Owing to their involvement in drug action these genes may further be potential targets for the modulation of drug sensitivity. |
17660802 |
Lnc2Cancer
|
cervical cancer |
qPCR etc. |
cell line (CaSki) |
up-regulated |
Interaction |
MALAT1 was involved in cervical cancer cell growth, cell cycle progression, and invasion through the regulation of gene expression, such as caspase-3, -8, Bax, Bcl-2, and BclxL. |
20213048 |
LncRNADisease Lnc2Cancer
|
lung adenocarcinoma |
qPCR etc. |
cell line (A549 ) |
differential expression |
interaction |
MALAT-1 is a novel class of non-coding RNA that promotes cell motility of lung adenocarcinoma cells through transcriptional and post-transcriptional regulation of motility related gene expression. |
20937273 |
LncRNADisease Lnc2Cancer
|
colorectal cancer |
qPCR etc. |
CRC tissue, cell lines (SW620, SW480 etc.) |
differential expression |
N/A |
The 3' end of MALAT-1 is an important biological motif in the invasion and metastasis of CRC cells. |
21503572 |
LncRNADisease Lnc2Cancer
|
non-small cell lung cancer |
qPCR etc. |
cell lines (A549, plat-E, HTB-58 etc.) |
up-regulated |
expression |
The long noncoding MALAT-1 RNA indicates a poor prognosis in non-small cell lung cancer and induces migration and tumor growth. |
22088988 |
LncRNADisease Lnc2Cancer
|
cervical cancer |
qPCR etc. |
cell line (CaSki) |
down-regulated |
N/A |
Generally, we found that some of the RNA molecules (HOTAIR and MALAT1) are down-regulated while many of them (lincRNA-p21, GAS5, MEG3, ANRIL, and ncRNA-CCND1) are up-regulated and some others (TUG1, UCA1, and PANDA) not affected. The decline in the expression of HOTAIR and MALAT1 was clearly evident in BLM-treated HeLa and MCF cells. For lincRNA-p21, ncRNA-CCND1, and MEG3, a similar up-regulation pattern was obvious in both cell lines where the increase was generally more pronounced in BLM-treated cells. |
22487937 |
LncRNADisease Lnc2Cancer
|
lung cancer |
qPCR etc. |
cell lines (A549, A549 MALAT1 KO, EBC-1 etc.) |
up-regulated |
regulation |
The noncoding RNA MALAT1 is a critical regulator of the metastasis phenotype of lung cancer cells. |
23243023 |
LncRNADisease Lnc2Cancer
|
prostate cancer |
qPCR etc. |
prostate cancer tissue, cell lines (22RV1, LNCAP-AI etc.) |
up-regulated |
N/A |
MALAT-1 was up-regulated in human prostate cancer tissues and cell lines. Higher MALAT-1 expression correlated with high Gleason score, prostate specific antigen, tumor stage and castration resistant prostate cancer. MALAT-1 down-regulation by siRNA inhibited prostate cancer cell growth, invasion and migration, and induced castration resistant prostate cancer cell cycle arrest in the G0/G1 phases. |
23845456 |
Lnc2Cancer
|
non-small cell lung cancer |
qPCR etc. |
NSCLC tissue |
up-regulated |
N/A |
MALAT1 was shown to be detectable in the cellular fraction of peripheral human blood, showing different expression levels between cancer patients and cancer-free controls. For the discrimination of NSCLC patients from cancer-free controls a sensitivity of 56% was calculated conditional on a high specificity of 96%. The results of this study indicate that MALAT1 complies with key characteristics of diagnostic biomarkers, i.e., minimal invasiveness, high specificity, and robustness. |
24313945 |
Lnc2Cancer
|
pituitary adenoma |
qPCR etc. |
pituitary adenomas tissue |
up-regulated |
expression |
Expression of the long non-coding RNAs MEG3, HOTAIR, and MALAT-1 in non-functioning pituitary adenomas and their relationship to tumor behavior. |
24469926 |
LncRNADisease Lnc2Cancer
|
multiple myeloma |
qPCR etc. |
blood (plasma) |
down-regulated |
expression |
HOTAIR long non-coding RNA is a negative prognostic factor not only in primary tumors, but also in the blood of colorectal cancer patients. |
24583225 |
LncRNADisease Lnc2Cancer
|
pancreatic ductal adenocarcinoma |
qPCR etc. |
PADC tissue, cell lines (Panc-1, Bxpc-3, HPDE6C-7 etc.) |
up-regulated |
N/A |
The relative level of MALAT1 was significantly higher in PDAC compared to the adjacent normal pancreatic tissues. When comparing the MALAT1 level in the cultured cell lines, remarkably higher expression of MALAT1 was found in aspc-1 PDAC cells compared with the immortal pancreatic duct epithelial cell line HPDE6c-7. Furthermore, MALAT1 expression level showed significant correlation with tumor size, tumor stage and depth of invasion. Kaplan-Meier analysis revealed that patients with higher MALAT1 expression had a poorer disease free survival. |
24815433 |
Lnc2Cancer
|
cervical cancer |
qPCR etc. |
cervical cancer tissue, cell lines (HeLa, CaSki, SiHa, HCC94 etc.) |
up-regulated |
N/A |
In the present study, it was identified that MALAT1 expression was upregulated in cervical cancer cell lines compared with normal cervical squamous cell samples. Further study into the effect of MALAT1 on cellular phenotype revealed that MALAT1 was able to promote cell migration and proliferation. HPV correlates with MALAT1 deregulation in cervical cancer. |
24932303 |
Lnc2Cancer
|
colorectal cancer |
qPCR etc. |
colorectal cancer tissue |
up-regulated |
regulation |
The MALAT1 levels in cancerous tissues were 2.26 times higher than those measured in noncancerous tissues, and this difference was statistically significant. Based on their expression level of MALAT1, the patients were divided into a high MALAT1 expression group and a low expression group. Patients with tumours harbouring higher expression of MALAT1 showed a significantly worse prognosis with a HR of 2.863 for DFS and 3.968 for OS. Furthermore, patients with perineural invasion demonstrated significantly worse DFS and OS than those without perineural invasion. |
25031737 |
Lnc2Cancer
|
laryngeal squamous cell carcinoma |
qPCR etc. |
LSCC tissue |
up-regulated |
expression |
We discovered that five lncRNAs were differentially expressed between primary LSCC samples and adjacent normal tissues. Among them, three lncRNAs were up-expressed in tumor specimens, including CDKN2B-AS1, HOTAIR and MALAT1. More, two lncRNAs had significant down-expression, which were lncRNA RRP1B and SRA1. Cisplatin and paclitaxel have target function on significant lncRNAs in LSCC, which presents novel molecular targets to cure LSCC patients and also leads an orientation for developing new drugs. |
25257554 |
Lnc2Cancer
|
multiple myeloma |
qPCR etc. |
Bone marrow |
up-regulated |
N/A |
MALAT1 was overexpressed in the newly diagnosed patients compared with post-treatment patients and healthy individuals. The expression of MALAT1 strongly correlated with disease status, and the magnitude of change in MALAT1 post-treatment had prognostic relevance. The patients with early progression had a significantly smaller change in MALAT1 after treatment. |
25369863 |
LncRNADisease Lnc2Cancer
|
pancreatic cancer |
qPCR etc. |
pancreatic cancer tissue |
up-regulated |
expression |
Our results indicated that lncRNA MALAT1 was highly expressed in pancreatic cancer compared with adjacent non-cancerous tissues, and positively correlated with clinical stage, tumor size, lymph node metastasis, and distant metastasis in pancreatic cancer patients. Furthermore, we also found that lncRNA MALAT1 overexpression was an unfavorable prognostic factor in pancreatic cancer patients, regardless of clinical stage, tumor size, lymph node metastasis, and distant metastasis. Finally, increased lncRNA MALAT1 expression was an independent poor prognostic factor for pancreatic patients through multivariate analysis. |
25481511 |
Lnc2Cancer
|
glioma |
qPCR etc. |
glioma tissue |
up-regulated |
expression |
LncRNA MALAT1 expression was increased in glioma tissues compared with paired adjacent brain normal tissues. Furthermore, lncRNA MALAT1 was associated significantly with WHO grade (I-II vs. III-IV; P = 0.007) and tumor size. Moreover, the level of lncRNA MALAT1 expression was markedly correlated with the glioma patients' overall survival. Multivariate analysis suggested that increased lncRNA MALAT1 expression was a poor independent prognostic predictor for glioma patients. |
25613066 |
Lnc2Cancer
|
gastric cancer |
qPCR etc. |
gastric cancer tissue, cell lines(AGS, MKN45, 7901 etc.) |
up-regulated |
expression |
All the 8 lncRNAs were then subjected to qPCR validation using 20 pairs of GC and control tissues. Among them, HOTAIR, PVT1, H19, MALAT1, GHET1 and HULC were significantly higher in tumor tissues compared with control tissues. |
26096073 |
Lnc2Cancer
|
lung cancer |
qPCR etc. |
blood |
down-regulated |
expression |
The expression of MALAT1 in the whole blood of lung cancer patients with metastasis was stronger compared to non-metastasis, which showed that MALAT1 promotes the tumor metastasis and additionally, the whole blood with lymph node metastasis represented a lower expression of MALAT1 compared to bone or brain metastasis. |
26137228 |
Lnc2Cancer
|
breast cancer |
qPCR etc. |
breast cancer and adjacent non-cancerous specimens, cell lines (MDA-MB-231 and MDA-MB-453) |
down-regulated |
interaction |
We found that MALAT1 was downregulated in breast tumor cell lines and cancer tissue, and showed that knockdown of MALAT1 in breast cancer cell lines induced an epithelial-to-mesenchymal transition (EMT) program via phosphatidylinositide-3 kinase-AKT pathways. Furthermore, lower expression of MALAT1 in breast cancer patients was associated with shorter relapse-free survival |
26191181 |
Lnc2Cancer
|
esophageal squamous cell carcinoma |
qPCR etc. |
ESCC tissue |
up-regulated |
expression |
MALAT1 expression was increased in ESCC tissue than in adjacent normal tissue samples (P< 0.001). MALAT1 level was positively related to pT stage (P= 0.01). |
26406400 |
Lnc2Cancer
|
renal cancer |
qPCR etc. |
clear cell renal cell carcinoma and corresponding noncancerous tissues |
up-regulated |
interaction |
We found that MALAT1 exist a higher fold change (Tumor/Normal) in clear cell kidney carcinoma (KIRC) from The Cancer Genome Atlas (TCGA) Data Portal and a negative correlation with miR-200s family. We further demonstrated MALAT1 promote KIRC proliferation and metastasis through sponging miR-200s in vitro and in vivo. In addition, miR-200c can partly reverse the MALAT1's stimulation on proliferation and metastasis in KIRC. In summary we unveil a branch of the MALAT1/miR-200s/ZEB2 pathway that regulates the progression of KIRC. |
26461224 |
Lnc2Cancer
|
colorectal cancer |
qPCR, in vitro knockdown, RIP etc. |
cell lines (LoVo, HCT116 ) |
up-regulated |
N/A |
We found that overexpression of MALAT1 could promote cell proliferation and migration in vitro, and promote tumour growth and metastasis in nude mice. In CRC, MALAT1 could bind to SFPQ, thus releasing PTBP2 from the SFPQ/PTBP2 complex. In turn, the increased SFPQ-detached PTBP2 promoted cell proliferation and migration. SFPQ critically mediated the regulatory effects of MALAT1. Moreover, in CRC tissues, MALAT1 and PTBP2 were overexpressed, both of which were associated closely with the invasion and metastasis of CRC. MALAT1 might be a potential predictor for tumour metastasis and prognosis.Furthermore, the interaction between MALAT1 and SFPQ could be a novel therapeutic target for CRC. |
25025966 |
Lnc2Cancer
|
endometrial stromal sarcoma |
qPCR, ISH etc. |
ESS tissue |
up-regulated |
expression |
MALAT-1 gene is one of the major genes upregulated in ESS. |
16441420 |
LncRNADisease Lnc2Cancer
|
cervical cancer |
qPCR, knockdown etc |
Tumor and adjacent normal tissues, cervical cancer cell lines(HeLa, CaSki) |
up-regulated |
expression |
MALAT1 expression is significantly increased in cervical cancer than in normal tissues. Its expression in the cancerous tissues is also significantly higher than in adjacent normal tissues. MALAT1 expression is correlated with tumor size, FIGO stage, vascular invasion and lymph nodes metastasis and is an independent predictor for overall survival of cervical cancer. When endogenous MALAT1 was knocked down, the cancer cells had significantly reduced proliferation and invasion and increased apoptosis |
26400521 |
Lnc2Cancer
|
hepatocelluar carcinoma |
qPCR, knockdown etc. |
HCC tissue |
up-regulated |
expression |
Long non-coding RNA MALAT-1 overexpression predicts tumor recurrence of hepatocellular carcinoma after liver transplantation. |
21678027 |
LncRNADisease Lnc2Cancer
|
urothelial carcinoma of the bladder |
qPCR, knockdown etc. |
cell lines (T24, 5737) |
up-regulated |
N/A |
MALAT1 was upregulated in bladder urothelial carcinoma compared with matched normal urothelium (P=.008). The MALAT1 expression levels were greater in high-grade carcinomas than in low-grade carcinoma (P=.001). The MALAT1 expression levels were greater in invasive carcinoma than in noninvasive carcinoma (P=.018). MALAT1 plays an oncogenic role in urothelial carcinoma of the bladder. |
23153939 |
Lnc2Cancer
|
melanoma |
qPCR, knockdown etc. |
melanoma tissue, cell line (A-375) |
up-regulated |
N/A |
highly expressed,can promote the metastasis of melanoma. The expression levels of UCA1 and Malat-1 lncRNAs had the potential to be prognostic indicators in metastasis of melanomas. |
24892958 |
Lnc2Cancer
|
gastric cancer |
qPCR, knockdown etc. |
gastric cancer tissue, cell lines (MKN7, MKN45, MKN74, NUGC4, AZ521, AGS, KATOIII) |
up-regulated |
interaction |
Expression of both lncRNAs was significantly higher in cancerous tissues than in corresponding normal mucosa, and higher expression of these lncRNAs significantly correlated with peritoneal metastasis in GC patients. Elevated HOTAIR expression emerged both as an independent prognostic and risk factor for peritoneal dissemination. SiRNA knockdown of HOTAIR in GC cells significantly inhibited cell proliferation, migration and invasion, but concurrently enhanced the anoikis rate in transfetced cells. |
25280565 |
Lnc2Cancer
|
clear cell renal cell carcinoma |
qPCR, knockdown etc. |
ccRCC tissue, cell line (HK-2) |
up-regulated |
expression |
The expression level of MALAT1 was higher in ccRCC tissues and renal cancer cells compared to adjacent non-tumor tissues and normal human proximal tubule epithelial cells HK-2. The ccRCC patients with higher MALAT1 expression had an advanced clinical features and a shorter overall survival time than those with lower MALAT1 expression. Additionally, our data indicated that knockdown expression of MALAT1 decreased renal cancer cell proliferation, migration, and invasion. |
25480417 |
Lnc2Cancer
|
esophageal squamous cell carcinoma |
qPCR, knockdown etc. |
esophageal squamous cell carcinoma and adjacent nonneoplastic tissues, cell lines(TE1, KYSE30, KYSE70, KYSE150, KYSE270, KYSE410, EC9706) |
up-regulated |
expression |
Human esophageal carcinoma cell lines EC9706 and KYSE150 were transfected with MALAT-1 small interference RNA. Cell proliferation, migration/invasion ability, cell cycle, and apoptosis were assessed. MALAT-1 expressed higher levels in esophageal cancer tissues when compared with paired adjacent normal tissues. This high expression was associated with a decreased survival rate. MALAT-1 knockdown induced a decrease in proliferation-enhanced apoptosis, inhibited migration/invasion, and reduced colony formation and led to cell cycle arrest at the G2/M phase |
26493997 |
Lnc2Cancer
|
osteosarcoma |
qPCR, knockdown etc. |
osteosarcoma tissue, cell lines (MG63, Saos-2, hFOB1.19, MNNG/HOS) |
up-regulated |
expression |
We observed that MALAT1 expression was up-regulated in human osteosarcoma cell lines and tissues. In vitro knockdown of MALAT1 by siRNA significantly inhibited cell proliferation and migration, and induced cell cycle arrest and apoptosis in osteosarcoma cells. In addition, MALAT1 knockdown markedly suppressed the formation of tubular network structures and caused breakage of stress fibers in osteosarcoma cell lines U2OS and MNNG/HOS. |
26575981 |
Lnc2Cancer
|
non-small cell lung cancer |
qPCR, knockdown, Luciferase reporter assay etc. |
NSCLC tissue, cell lines (A549, YTLMC-9) |
up-regulated |
interaction |
MALAT1 is a non-coding RNA overexpressed in non-small cell lung cancer (NSCLC). TDP-43 is a ubiquitously expressed, MALAT1-binding protein implicated in cancer development. TDP-43 overexpression markedly increased MALAT1 transcript level. In summary, these findings demonstrated that MALAT1 expression by regulation of TDP-43 controls cellular growth, migration, and invasion of NSCLCs. |
26265046 |
Lnc2Cancer
|
esophageal squamous cell carcinoma |
qPCR, Luciferase reporter assay etc. |
ESCC tissue, cell lines (KYSE30, KYSE150, KYSE450) |
up-regulated |
regulation |
In this study, we provide first evidences that a posttranscriptional regulation mechanism of MALAT1 by miR-101 and miR-217 exists in ESCC cells. This posttranscriptional silencing of MALAT1 could significantly suppress the proliferation of ESCC cells through the arrest of G2/M cell cycle, which may be due to MALAT1-mediated upregulation of P21 and P27 expression and the inhibition of B-MYB expression. |
25538231 |
Lnc2Cancer
|
renal cell carcinoma |
qPCR, Luciferase reporter assay etc. |
RCC tissue |
up-regulated |
N/A |
Long Noncoding RNA MALAT1 Promotes Aggressive Renal Cell Carcinoma through Ezh2 and Interacts with miR-205. MALAT1 expression was higher in human RCC tissues, where it was associated with reduced patient survival. |
25600645 |
LncRNADisease Lnc2Cancer
|
multiple myeloma |
qPCR, Luciferase reporter assay, ELISA, knockdown etc. |
bone marrow |
up-regulated |
expression |
The expression of MALAT1 was assessed by quantitative qPCR. Consistently higher expression level of MALAT1 was found in MSCs from all 25 patient samples relative to that from healthy donors. lncRNA MALAT1 directly interacted with Sp1 and LTBP3 promoter to increase expression of LTBP3 gene. The specificity and efficiency of activation were ensured by the formation of a stable complex between MALAT1 and the LTBP3 promoter, direct interaction of MALAT1 with Sp1 and recruitment of Sp1 to the promoter. |
25187517 |
Lnc2Cancer
|
cervical cancer |
qPCR, Luciferase reporter assays, knockdown, RIP, RNA pull-down assay etc. |
cervical cancer tissue, cell lines (HeLa and CaSki) |
up-regulated |
interaction |
We found MALAT1 expression was significantly higher in radioresistant than in radiosensitive cancer cases. In addition, MALAT1 and miR-145 expression inversely changed in response to irradiation in HR-HPV+ cervical cancer cells. By using clonogenic assay and flow cytometry analysis of cell cycle distribution and apoptosis, we found CaSki and Hela cells with knockdown of MALAT1 had significantly lower colony formation, higher ratio of G2/M phase block and higher ratio of cell apoptosis. |
26311052 |
Lnc2Cancer
|
lung cancer |
qPCR, Northern blot, etc. |
cell lines (H1299, H1975 etc.) |
differential expression |
N/A |
We first examined the decay of MALAT-1 in various cancer cells (H1299, H1975, A549, HT1080, and HeLa TO cells) by DRB chase experiments using 7SK RNA as a control. Half-lives of MALAT-1 in H1299, H1975, A549, HT1080, and HeLa TO cells were > 12, 12, 12, 12, and 9 h, respectively. MALAT-1 stabilities varied in various cancer cells. |
22491206 |
Lnc2Cancer
|
fibrosarcoma |
qPCR, Northern blot, etc. |
cell line (HT1080) |
differential expression |
N/A |
We first examined the decay of MALAT-1 in various cancer cells (H1299, H1975, A549, HT1080, and HeLa TO cells) by DRB chase experiments using 7SK RNA as a control. Half-lives of MALAT-1 in H1299, H1975, A549, HT1080, and HeLa TO cells were > 12, 12, 12, 12, and 9 h, respectively. MALAT-1 stabilities varied in various cancer cells. |
22491206 |
Lnc2Cancer
|
cervical cancer |
qPCR, Northern blot, etc. |
cell line (HeLa) |
differential expression |
N/A |
We first examined the decay of MALAT-1 in various cancer cells (H1299, H1975, A549, HT1080, and HeLa TO cells) by DRB chase experiments using 7SK RNA as a control. Half-lives of MALAT-1 in H1299, H1975, A549, HT1080, and HeLa TO cells were > 12, 12, 12, 12, and 9 h, respectively. MALAT-1 stabilities varied in various cancer cells. |
22491206 |
Lnc2Cancer
|
hepatocelluar carcinoma |
qPCR, Northern blot, ISH etc. |
HCC tissue, cell line (CT26) |
up-regulated |
expression |
Quantitative analyses indicated a 6-7-fold increased RNA level in HCCs versus uninvolved liver, advancing this as a molecule of interest. |
16878148 |
LncRNADisease Lnc2Cancer
|
prostate cancer |
qPCR, Northern bolt etc. |
prostate cancer tissue, cell lines (LNCap-AD, 22Rv1, PC-3, DU145, C4-2 etc.) |
up-regulated |
N/A |
qPCR was used to assess the PCA3 and MALAT-1 expression levels in an additional set of 10 pairs of PCa and adjacent normal tissues. Comparing the PCA3 and MALAT-1 expression levels in the 10 paired tissue samples revealed that PCA3 and MALAT-1 were highly expressed in most of the PCa tissues. Plasma lncRNAs probably exist in the form of fragments in a stable form. MD-miniRNA enters cell culture medium at measurable levels, and MD-miniRNA derived from human PCa xenografts actually enters the circulation in vivo and can be measured to distinguish xenografted mice from controls. |
23726266 |
Lnc2Cancer
|
prostate cancer |
qPCR, RIP-Seq, knockdown, ChIP etc. |
cell lines (C4-2, PC-3, LNCaP) |
up-regulated |
interaction |
We showed that MALAT1 enhances expression of PRC2-independent target genes of EZH2 in CRPC cells in culture and patient-derived xenografts. Together, these data indicate that MALAT1 may be a crucial RNA cofactor of EZH2 and that the EZH2-MALAT1 association may provide a new avenue for development new strategies for treatment of CRPC. |
26516927 |
Lnc2Cancer
|
gallbladder cancer |
qPCR, Western blot etc. |
GBC tissue, cell lines (SGC-996, NOZ) |
up-regulated |
regulation |
MALAT1 promotes the proliferation and metastasis of gallbladder cancer cells by activating the ERK/MAPK pathway. |
24658096 |
LncRNADisease Lnc2Cancer
|
non-small cell lung cancer |
qPCR, Western blot etc. |
NSCLC tissue, cell lines (H1915) |
up-regulated |
expression |
We observed that the level of MALAT1 was significantly higher in brain metastasis than that of non brain metastasis samples. The level of MALAT1 was associated with patients' survival. We found that MALAT1 is increased in highly invasive subline of brain metastasis lung cancer cells. Further functional studies indicate that silencing MALAT1 inhibits highly invasive subline of brain metastasis lung cancer cell migration and metastasis by inducing epithelial-mesenchymal transition (EMT). |
25217850 |
Lnc2Cancer
|
pancreatic cancer |
qPCR, Western blot etc. |
cell lines (AsPC-1, CFPAC-1) |
up-regulated |
expression |
In this study, our data showed that MALAT-1 could increase the proportion of pancreatic CSCs, maintain self-renewing capacity, decrease the chemosensitivity to anticancer drugs, and accelerate tumor angiogenesis in vitro. In addition, subcutaneous nude mouse xenografts revealed that MALAT-1 could promote tumorigenicity of pancreatic cancer cells in vivo. The underlying mechanisms may involve in increased expression of self-renewal related factors Sox2. |
25811929 |
Lnc2Cancer
|
pancreatic cancer |
qPCR, Western blot, FCA etc. |
pancreatic cancer tissue, cell lines (BxPC-3, CFPAC-1, CAPAN-1, SW1990 etc.) |
up-regulated |
expression |
In the present study, our results showed that MALAT-1 expression levels were upregulated in pancreatic cancer tissues compared with adjacent noncancerous controls. Further function analysis revealed that downregulation of MALAT-1 could inhibit tumor cell proliferation and decrease cell migration and invasion in vitro. |
25269958 |
Lnc2Cancer
|
gastric cancer |
qPCR, Western blot, knockdown etc. |
cell lines (SGC-7901, MKN-45, SUN-16) |
up-regulated |
N/A |
In this study, we found that MALAT1 was aberrantly highly expressed in GC cell lines (SGC-7901, MKN-45 and SUN-16), and induced specific distribution and over-expression of SF2/ASF in nucleolus. Knock-down of MALAT1 or SF2/ASF in SGC-7901 cells respectively induced significant arrest of cell cycle in G0/G1 phase along with a remarkable suppression of cell proliferation, and the nuclear distribution and expression of SF2/ASF was significantly impaired when MALAT1 was depleted. However, over-expression of SF2/ASF exhibited no effect on rescuing the cell proliferation suppression by MALAT1 depletion. |
24857172 |
Lnc2Cancer
|
osteosarcoma |
qPCR, Western blot, knockdown etc. |
osteosarcoma tissue, cell lines (SAOS2, MG63, U2OS) |
up-regulated |
expression |
In our research, the MALAT1 messenger RNA (mRNA) was highly expressed in human osteosarcoma tissues, and its expression level was closely correlated with pulmonary metastasis. Knockdown of MALAT1 inhibited the proliferation and invasion of human osteosarcoma cell and suppressed its metastasis in vitro and vivo. MALAT1 might suppress the tumor growth and metastasis via PI3K/AKT signaling pathway. |
25431257 |
Lnc2Cancer
|
esophageal squamous cell carcinoma |
qPCR, Western blot, knockdown etc. |
ESCC tissue, cell lines (EC109, EC9706, KYSE150, KYSE450) |
up-regulated |
expression |
MALAT1 was over-expressed in 46.3% of ESCC tissues, mostly in the high-stage tumor samples. Enhanced MALAT1 expression levels were positively correlated with clinical stages, primary tumor size, and lymph node metastasis. Inhibition of MALAT1 suppressed tumor proliferation in vitro and in vivo, as well as the migratory and invasive capacity.MALAT1 serves as an oncogene in ESCC, and it regulates ESCC growth by modifying the ATM-CHK2 pathway. |
25613496 |
Lnc2Cancer
|
oral squamous cell carcinoma |
qPCR, Western blot, knockdown etc. |
OSCC tissue, cell lines (Tscca, Tca8113P160, Tca8113, Hep-2) |
up-regulated |
interaction |
We found that MALAT1 is overexpressed in OSCC tissues compared to normal oral mucosa by real-time PCR. MALAT1 served as a new prognostic factor in OSCC patients. When knockdown by small interfering RNA (siRNA) in OSCC cell lines TSCCA and Tca8113, MALAT1 was shown to be required for maintaining epithelial-mesenchymal transition (EMT) mediated cell migration and invasion. Western blot and immunofluorescence staining showed that MALAT1 knockdown significantly suppressed N-cadherin and Vimentin expression but induced E-cadherin expression in vitro. Meanwhile, both nucleus and cytoplasm levels of β-catenin and NF-B were attenuated, while elevated MALAT1 level triggered the expression of β-catenin and NF-B. More importantly, targeting MALAT1 inhibited TSCCA cell-induced xenograft tumor growth in vivo. |
26522444 |
Lnc2Cancer
|
cervical cancer |
qPCR, Western blot, Luciferase reporter assay, knockdown, FCA etc. |
HR-HPV+ cervical cancer tisssue, cell lines (HeLa, CaSki, SiHa) |
up-regulated |
interaction |
Findings of this study confirmed higher MALAT1 expression in HR-HPV (+) cervical cancer. Knockdown of endogenous MALAT1 significantly reduced cell growth rate and invasion and increased cell apoptosis of Hela and siHa cells. Besides, knockdown of MALAT1 increased the expression of miRNA-124, while ectopic expression of miR-124 decreased MALAT1 expression. MALAT1 can indirectly modulate GRB2 expression via competing miR-124. Knockdown of GRB2 reduced cell invasion and increased cell apoptosis. In conclusion, MALAT1 can promote HR-HPV (+) cancer cell growth and invasion at least partially through the MALAT1-miR-124-RBG2 axis. |
26242259 |
Lnc2Cancer
|
colorectal cancer |
qPCR, Western blot, Luciferase reporter assay, knockdown, RIP etc. |
CRC tissue, cell lines (LoVo etc.) |
up-regulated |
N/A |
Using in situ hybridization, we found there was higher expression of MALAT1 in the CRC than the adjacent normal colorectal tissue. We next conducted correlation analysis between MALAT1 expression and clinicopathological characteristics of CRC. A statistically significant association was observed between MALAT1 expression and extent of metastasis and invasion. In contrast to adjacent normal tissues, the MALAT1 expression in CRC tissues resected from patients with metastatic diseases was higher than those with no metastasis. |
24244343 |
Lnc2Cancer
|
bladder cancer |
qPCR, Western blot, Luciferase reporter assay, knockdown, RIP etc. |
bladder cancer tissue, cell lines (T24, RT4 etc.) |
up-regulated |
N/A |
TGFβ1 induces malat1 expression and EMT in bladder cancer cells. malat1 overexpression is significantly correlated with poor survival in patients with bladder cancer. malat1 and E-cadherin expression is negatively correlated in vitro and in vivo. malat1 knockdown inhibits TGFβ1 induced EMT. malat1 is associated with suz12, and this association results in decrease of E-cadherin expression and increase of N-cadherin and fibronectin expression. Targeted inhibition of malat1 or suz12 suppresses the migratory and invasive properties induced by TGFβ1 We demonstrated that malat1 or suz12 knockdown inhibits tumor metastasis in animal models. |
24449823 |
Lnc2Cancer
|
breast cancer |
qPCR, Western blot, Luciferase reporter assays etc. |
breast cancer patients tissues |
down-regulated |
interaction |
The effects of up-regulation of miR-1 were similar to that of silencing K-RAS and MALAT1 in breast cancer cells |
26275461 |
Lnc2Cancer
|
nasopharyngeal carcinoma |
qPCR, Western blot, Luciferase reporter assays, RIP etc. |
NPC cell lines (5-8F, CNE-2, HONE-1, SUNE-1), NPE cell line (NP-69) |
up-regulated |
interaction |
We found that MALAT1 regulated radioresistance by modulating cancer stem cell (CSC) activity. Furthermore, we found that there was reciprocal repression between MALAT1 and miR-1, and slug was identified as a downstream target of miR-1. Taking these observations into consideration, we proposed that MALAT1 regulated CSC activity and radioresistance by modulating miR-1/slug axis, which indicated that MALAT1 could act as a therapeutic target for NPC patients |
26482776 |
Lnc2Cancer
|
breast cancer |
qPCR, Western blot, Luciferase reporter assays, RIP etc. |
breast cancer specimens and adjacent normal breast tissue |
up-regulated |
interaction |
We reported that MALAT1 was upregulated in triple-negative breast cancer (TNBC) tissues. Knockdown of MALAT1 inhibited proliferation, motility, and increased apoptosis in vitro. In vivo study indicated that knockdown of MALAT1 inhibited tumor growth and metastasis. Patients with high MALAT1 expression had poorer overall survival time than those with low MALAT1 expression. In addition, our findings demonstrate a reciprocal negative control relationship between MALAT1 and miR-1: downregulation of MALAT1 increased expression of microRNA-1 (miR-1), while overexpression of miR-1 decreased MALAT1 expression. Slug was identified as a direct target of miR-1. |
26676637 |
Lnc2Cancer
|
glioma |
qPCR, Western blot, Luciferase reporter assays, RIP, ChIP etc. |
glioma samples and normal brain tissues, cell lines (hCMEC/D3, ECs) |
up-regulated |
interaction |
Our results proved that MALAT1 expression was up-regulated in brain microvessels of human glioma and glioma endothelial cells (GECs) which were obtained by co-culturing endothelial cells with glioma cells. Functionally, knockdown of MALAT1 resulted in an impairment and increased the permeability of BTB as well as decreased the expression of ZO-1, occludin and claudin-5 in GECs. Further, there was reciprocal repression between MALAT1 and miR-140, and miR-140 mediated the effects that MALAT1 knockdown exerted. Mechanistic investigations defined that nuclear factor YA (NFYA), a CCAAT box-binding transcription factor, was a direct and functional downstream target of miR-140, which was involved in the MALAT1 knockdown induced regulation of BTB function. Furthermore, NFYA could up-regulate the promoter activities and bind to the promoters of ZO-1, occludin and claudin-5 in GECs. |
26619802 |
Lnc2Cancer
|
breast cancer |
qPCR, Western blot, Northern blot, knockdown etc. |
cell lines (MB231, MCF7 etc.) |
up-regulated |
N/A |
Specifically, we looked for the changes of long non-coding RNA metastasis associated lung adenocarcinoma transcript 1 (MALAT-1), which is found extensively and highly expressed in several kinds of tumor cells, including breast carcinoma. It was observed that proliferation, migration and invasion of breast cells were greatly affected by high concentration E2 treatment and were not affected by low concentration E2 treatment in an ERa independent way. We found that the high concentration E2 treatment largely decreased MALAT-1 RNA level. Interestingly, MALAT-1 decreasing by knocking down showed similar effects on proliferation, migration and invasion. |
24525122 |
Lnc2Cancer
|
nasopharyngeal carcinoma |
qPCR, Western bolt etc. |
cell lines (5-8F, 6-10B, CNE-1, CNE-2 etc.) |
up-regulated |
N/A |
MALAT1 was highly expressed in 5-8F cells with a high metastatic potential, and lowly expressed in normal nasopharyngeal epithelium cells. Overexpression of MALAT1 by RNAa suppressed the expression of E-cadherin, promoted the expression of vimentin and enhanced the proliferation, invasion, and metastasis of CNE-1 cells. |
23688988 |
Lnc2Cancer
|
bladder cancer |
qPCR, Western bolt, Luciferase reporter assay etc. |
bladder cancer tissue, cell line (T24) |
up-regulated |
N/A |
We verified that MALAT-1 levels were upregulated in bladder cancer tissues compared with adjacent normal tissues, and MALAT-1 expression was remarkably increased in primary tumors that subsequently metastasized, when compared to those primary tumors that did not metastasize. levels. We further demonstrated that MALAT-1 promoted EMT by activating Wnt signaling in vitro. |
22722759 |
Lnc2Cancer
|
esophageal squamous cell carcinoma |
qRT-PCR |
106 paired ESCC tissues |
down-regulated |
N/A |
MALAT1 decreased tumor formation and improved survival |
27015363 |
|
gastric cancer |
RNA immunoprecipitation RIP-seq |
gastric cancer cell lines |
N/A |
N/A |
suppresses the tumor suppressor PCDH10 and promotes gastric cellular migration and invasion |
26871474 |
|
prostate cancer |
RNA-seq, qPCR etc. |
prostate cancer tissue |
up-regulated |
N/A |
Consistent with the RNA-seq results, PCA3, FR0348383 and MALAT1 overexpression was found in 80% (32/40), 72.5% (29/40), and 82.5% (33/40) of the prostate cancers respectively, whereas decreased FR0257520 expression was found in 82.5% (33/40) of the prostate cancers. |
22349460 |
Lnc2Cancer
|
pre-eclampsia |
short interfering RNA (siRNA) |
placentas from the patients with preeclampsia, EG-3 trophoblast cell line |
down-regulated |
interaction |
Silencing of MALAT-1 in JEG-3 cells suppressed proliferation and induced cell cycle arrest at G0/G1 phase. The migration rate and the invasiveness of JEG-3 cells were suppressed when MALAT-1 was downregulated. MALAT-1 may play an important role in the regulation of proliferation, cell cycle, apoptosis, migration and invasion of trophoblast cells, and under-expression of MALAT-1 during early placentation may be involved in the pathogenesis of preeclampsia. |
26722461 |
|
triple-negative breast cancer |
tissue microarray; immunoblotting, polymerase chain reaction, loss and gain of gene |
MDA-MB-231 cells |
up-regulated |
N/A |
N/A |
26917489 |
|
|