RAMS11 promotes CRC through mTOR-dependent inhibition of autophagy, suppression of apoptosis, and promotion of epithelial-mesenchymal transition

Abstract Background Long non-coding RNAs (lncRNAs), a class of (ncRNAs) associated with diverse biological processes cells. Over the past decades, cumulating research evidences revealed that abnormal expressions lncRNAs are colorectal cancer (CRC) initiation, progression, metastasis, and resistance to therapies. Moreover, their usefulness as candidate biomarkers for CRC diagnosis prognosis well evident throughout previous literature. In current study, we examined role molecular mechanisms newly identified lncRNA named RNA metastasis-11 (RAMS11) in development. Methods The expression RAMS11 cell lines DLD-1, HT-29, HCT-116, SW480 colon normal cells CCD-112-CoN were evaluated by quantitative RT-qPCR. results showed is significantly upregulated compared CCK-8 proliferation assay, colony formation migration assay performed evaluate physiological functions vitro. To decipher medicated further western blot analysis key pathway proteins (e.g., AMPK, AKT, mTOR). Results Our higher increased proliferation, migration, development metastasis. Knockdown induced autophagy, apoptosis along reduction epithelial-mesenchymal transition (EMT) suggesting involved progression. indicated knockdown inhibited carcinogenesis through mTOR-dependent autophagy induction. Conclusions sum, our suggested an important oncogene pathogenesis. Targeting could be potential therapeutic strategy management.