RESULTS MALAT1 mRNA was upregulated in NSCLC tissues and cell lines compared to that in adjacent tissues and normal human bronchial cell line (BEAS-2B), respectively.
However, the biomechanism through which METTL3 regulates MALAT1-miR-1914-3p-YAP axis activity to induce NSCLC drug resistance and metastasis is not very clear.
Taken together, our study makes clear that miR-142-3p functions as a tumor suppressor in NSCLC progression through inhibiting MALAT1/β-catenin signaling.
LncRNA MALAT-1 expression was higher in NSCLC tissues than that in adjacent tissues, but a lower expression of miR-124 was detected in the former tissues than in the latter tissues.
Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) has been identified as a prognostic marker for the metastasis of early-stage non-small cell lung cancer (NSCLCs).
Recent studies have demonstrated that MALAT1 is involved in cancer metastasis and recurrence and it is up-regulated in cervical cancer, hepatocellular carcinoma, non-small cell lung cancer (NSCLC) and colorectal cancer.
We tested the expression of 11 candidate miRNAs and MALAT1 in a training set (36 NSCLCs vs. 36 controls) by quantitative reverse transcription polymerase chain reactions.
We also showed that MALAT1 promoted epithelial-mesenchymal transition, cell migration, and invasion by activating Akt/mTOR signaling in A549 and H1299 cells. miR-206 was a direct downstream target of MALAT1 in NSCLC.
Downregulation of MALAT1 may promote apoptosis and suppress proliferation, migration and invasion of human NSCLC A549 cells by inhibiting autophagy, thereby suppressing the development of NSCLC.
Here we demonstrate a novel role of Malat1, a long noncoding RNA that has been originally identified as a prognostic marker for non-small cell lung cancer, in cerebrovascular pathogenesis of ischemic stroke.
Finally, the NSCLC mice models were observed with larger tumor size and weight under circumstances of over-expressed MALAT1 and miR-197-3p, or under-expressed p120-ctn (<i>P</i> < 0.05).
Taken together, this study shed a light on utilizing MALAT-1 in exosomes as a non-invasive serum-based tumor biomarker for diagnosis and prognosis of NSCLC.
However, due to its low specificity, MALAT1 positive cases need further validation for NSCLC by other diagnostic methods such as radiology, cytology, etc.
In the present study, it was identified that metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), a long non-coding RNA that has been demonstrated to function as an oncogene, was increased in tumor tissues from patients with cisplatin-resistant NSCLC.
The lncRNAs HOTAIR, H19 and MALAT1 were up-regulated, while PANDAR and TUG1 were down-regulated in NSCLC cancer tissues compared with the corresponding adjacent normal tissue.
Overall, our findings illuminate the oncogenic function of MALAT1 which is regulated by DNA methylation that might provide potential clinical application in NSCLC.