FAM83A-AS1 Promotes Tumor Progression Through MET Signaling in Lung Adenocarcinoma

Abstract Background Studies demonstrate that long non-coding RNAs (lncRNAs) play critical roles in the occurrence and development of cancer. However, many of the molecular mechanisms underlying lncRNAs role in this process remains unclear. Methods Here, we analyzed lncRNA expression in lung cancer tissues based on RNA-Seq analysis and found that lncRNA FAM83A-AS1 was one of the top up-regulated lncRNAs in lung adenocarcinoma and elevated expression of FAM83A-AS1 was significantly associated with poor patient survival. We validated these results using RT-PCR and an independent cohort of lung cancer. Results Functional studies indicated that knockdown of FAM83A-AS1 decreased cell proliferation, colony formation, migration and invasion in H1299 and H838 lung cancer cells. Knockdown of FAM83A-AS1 induced the autophagy and cell cycle arrest at G2. Mechanistically, we found that MET, p62 and phosphor S6K proteins were decreased upon FAM83A-AS1 knockdown. Conclusion In conclusion, FAM83A-AS1 may have potential as a diagnosis/prognosis marker and its oncogenic role could lead to potential targeting for lung cancer therapy.