FAM83A antisense RNA 1 () silencing impairs cell proliferation and induces autophagy via MET-AMPKɑ signaling in lung adenocarcinoma.

Studies demonstrate that long non-coding RNAs (lncRNAs) play vital roles in cancer progression. However, the expression pattern and molecular mechanisms of lncRNA in lung cancer remain largely unclear. Here, we analyzed expression in lung cancer tissues from three RNA-sequencing (RNA-Seq) datasets and validated these results using quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR) in an independent set of lung adenocarcinoma. Cell proliferation, migration, invasion, and autophagy were analyzed after knockdown with siRNAs. The underlying molecular mechanisms of were performed by Western blot, qRT-PCR, and RNA-seq analysis. We found that was up-regulated in lung cancer and elevated expression was associated with poor patient survival. These results were confirmed using RT-PCR in an independent set of lung cancer. Functional study indicated that knockdown reduced cell proliferation, migration, invasion, and colony formation in cancer cells. silencing induced autophagy and cell cycle arrest at G2. Mechanistically, serval oncogenic proteins such as EGFR, MET, PI3K, and K-RAS were decreased upon silencing, while phosphor AMPKα and ULK1 were increased. Based on the above results, we believe that may have potential as a diagnosis/prognosis marker and its oncogenic role and autophagy regulation may be through MET-AMPKα signaling, which could lead to potential targeting for lung cancer therapy.