The expression of the long ncRNA MALAT1 correlates with tumor development, progression or survival in lung, liver and breast cancer.

Studies indicate the correlation of differential expression of metastasis-associated lung adenocarcinoma transcript1 (MALAT1) with tumor development, progression or survival in several cancerous conditions.

Our results suggest that MALAT-1 transcript induces migration in Non-small cell lung cancers and stimulates tumor growth and invasion in vivo.

The quantitative loss of MALAT1 did neither affect proliferation nor cell cycle progression nor nuclear architecture in human lung or liver cancer cells.

The noncoding RNA MALAT1 is a critical regulator of the metastasis phenotype of lung cancer cells.

The levels of plasma lncRNAs, H19, HOX antisense intergenic RNA (HOTAIR), and metastasis associated lung adenocarcinoma transcript-1 (MALAT1), were analyzed in patients with gastric cancer (GC) and healthy controls.

Results showed that the high level of MALAT1 is associated with lung cancer brain metastasis and survival and demonstrated the potential role of MALAT1 in identification of non-small cell lung cancer patients at high risk of brain metastasis

The data suggest that upregulation of MALAT1 was mediated by the transcription factor Sp1 in A549 lung cancer cells

MALAT1 expression by regulation of TDP-43 controls cellular growth, migration, and invasion of non-small cell lung cancer cells in vitro.

Posttranscriptional silencing of MALAT1 by miR-217 provides a link, through EZH2, between ncRNAs and the EMT and establishes a mechanism for cigarette smoke extract-induced lung carcinogenesis.

EZH2 is recruited to the E-cadherin promoter by the long non-coding RNA, MALAT-1 (metastasis associated in lung adenocarcinoma transcript 1), where it represses E-cadherin expression

MALAT1 expression in non-small cell lung cancer cells is regulated by DNA methylation.

Overexpression of Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) caused significant reduction in cell proliferation and invasion in vitro, and tumorigenicity in both subcutaneous and intracranial human glioma xenograft models.

The knockdown ofmetastasis-associated lung adenocarcinoma transcription 1 increased apoptosis rate of the two cell line and the expression levels of some tumor markers were reduced such as CCND1 and MYC.

MALAT1 regulated 153 miRNAs in lung cancer.

the present study found that MALAT1 was significantly highly expressed in non-small cell lung cancer (NSCLC) tissues with bone metastasis and in NSCLC cell lines with high bone metastatic ability

The rs3200401 T allele located on the lncRNA MALAT1 was associated with a better survival for advanced lung adenocarcinoma patients, which may offer a novel prognostic biomarker for this patient subgroup.

these results suggested that Axl, which is regulated by long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1, may exert great influence on invasion and migration of neuroblastoma

MALAT1 expression is controlled by Oct4 transcriptional regulation in lung cancer.

MALAT-1 expression is upregulated in the serum, and circulating exosomes of non-small cell lung cancer patients.

Notably, sirtuin 1 was recognized as a direct downstream target of microRNA-204 in HepG2 cells. Moreover, si-SIRT1 significantly inhibited cell invasion and migration process.his study reveals a novel mechanism by which MALAT1 stimulates hepatocellular carcinoma progression and justifies targeting metastasis-associated lung adenocarcinoma transcript 1 as a potential therapy for hepatocellular carcinoma.

Studied effects of lin-28 homolog A protein (Lin28A) on cells proliferation, migration, invasion and apoptosis of osteocarcinoma (OS) cells through metastasis associated lung adenocarcinoma transcript 1 (MALAT1).

Overexpression of MALAT1 contributed to cisplatin resistance in a lung cancer tumor cell line.

Data found that overexpression of the malat1 M5 fragment promoted proliferation, invasion and migration in vitro of human adenocarcinomic cells A549 and H1299, and stimulated tumor growth in mice in vivo. These results provide evidence that malat1 interacts with SP1 protein and promotes SP1-mediated transcriptional regulation of SP1 target genes in lung adenocarcinoma cells.

Results find MALAT1 highly expressed in non-small cell lung cancer (NSCLC) tissues, and positively correlates with that of SOX9.

Long non-coding RNA (lncRNA) MALAT1 (metastasis-associated lung adenocarcinoma transcript 1 rs4102217 polymorphism-smoking-drinking was the best interaction model, which has higher risk of coronary artery disease (CAD).

This study was aimed to explore if lncRNA MALAT1 would modify chemo-resistance of non-small cell lung cancer (NSCLC) cells by regulating miR-197-3p and p120 catenin (p120-ctn).

The expression of miR-20b-5p is negatively correlated with that of metastasis-associated lung adenocarcinoma transcript-1 (MALAT1, r = -0.928, p = 0.023) and Oct4 (r = -0.894, p = 0.041) in colorectal cells.

MicroRNA-497 (miR-497) post-transcriptionally represses metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) while MALAT1 competes for miR-497 binding to its molecular target, EIF4E (eukaryotic translation initiation factor 4E) in adrenocortical carcinoma. Overexpression of miR-497 and silencing of MALAT1 suppress cellular proliferation and induce cell cycle arrest through downregulation of EIF4E expression.

In this study, we demonstrated that in non-small cell lung cancer (NSCLC) tissues, the expression level of MALAT1 was negatively correlated with that of miR-200a-3p, while positively correlated with PD-L1. MALAT1 promoted proliferation, mobility, migration, and invasion of NSCLC cells via sponging miR-200a-3p.

High MALAT1 expression promotes the proliferation, migration, and invasion of non-small cell lung cancer via the ERK/MAPK signaling pathway.

Long noncoding RNA MALAT1 as a candidate serological biomarker for the diagnosis of non-small cell lung cancer: A meta-analysis.

Correlation Between Single Nucleotide Polymorphisms of the rs664589 Locus in the Long-Chain Noncoding RNA lung Adenocarcinoma Metastasis-Associated Gene 1, Hypertension, and Its Mechanism.

Extracellular Vesicle lncRNA Metastasis-Associated lung Adenocarcinoma Transcript 1 Released From Glioma Stem Cells Modulates the Inflammatory Response of Microglia After Lipopolysaccharide Stimulation Through Regulating miR-129-5p/High Mobility Group Box-1 Protein Axis.

Aberrantly elevated levels of metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) are detected in both hepatocellular carcinoma (HCC) specimens and cell lines. Cooperating with enhancer of zeste homolog 2 (EZH2), MALAT1 positively regulated snail family transcriptional repressor 1 (SNAI1) by repressing miR-22 and inhibiting E-cadherin expression, playing a vital role in epithelial to mesenchymal transition.

Long non-coding RNA MALAT1 regulates proliferation, apoptosis, migration and invasion via miR-374b-5p/SRSF7 axis in non-small cell lung cancer.

Long Non-Coding RNA Metastasis Associated lung Adenocarcinoma Transcript 1 (MALAT1) Promotes Hypertension by Modulating the Hsa-miR-124-3p/Nuclear Receptor Subfamily 3, Group C, Member 2 (NR3C2) and Hsa-miR-135a-5p/NR3C2 Axis.

Long-Chain Non-Coding RNA Metastasis-Related lung Adenocarcinoma Transcript 1 (MALAT1) Promotes the Proliferation and Migration of Human pulmonary Artery Smooth Muscle Cells (hPASMCs) by Regulating the MicroRNA-503 (miR-503)/Toll-Like Receptor 4 (TLR4) Signal Axis.

Targeting MALAT1 induces DNA damage and sensitize non-small cell lung cancer cells to cisplatin by repressing BRCA1.

Prognostic and clinicopathological significance of long noncoding RNA MALAT-1 expression in patients with non-small cell lung cancer: A meta-analysis.

MALAT1 rs619586 A/G polymorphisms are associated with decreased risk of lung cancer.