LncRNA SNHG6 inhibits autophagy of gastric carcinoma cells via PI3K/AKT/mTOR signaling pathway

Objective: To investigate the role of lncRNA SNHG6 (SNHG6) in gastric carcinoma (GC) and its relationship with the PI3K/AKT/mTOR signaling pathway in order to provide more comprehensive and reliable reference for the diagnosis and treatment of GC.

Methods: GC patients admitted to our hospital from May 2017 to August 2018 as well as healthy individuals who underwent physical examinations during the same time period were enrolled in this study. The serum SNHG6 level was quantified. Patients were followed up for 3 years to analyze the significance of SNHG6 in the diagnosis and treatment of GC. Finally, in vitro assays were performed to determine the influences of SNHG6 and PI3K/AKT/mTOR signaling pathway on biological behaviors and autophagy ability of GC cells.

Results: SNHG6 showed high expression in patients with GC and its expression decreased after therapy. SNHG6 also demonstrated a favorable predictive value for the development of GC and the death of patients. The survival curve suggested that increased SNHG6 indicated a higher risk of death. Additionally, mRNA of PI3K/AKT/mTOR pathway related molecules was highly expressed in GC patients. In in vitro assays, GC cells showed stronger viability and invasion activity and weaker apoptosis and autophagy ability after targeted up-regulation of SNHG6. According to the rescue assay, the effect of up-regulating SNHG6 on GC cells could be completely reversed by suppressing the PI3K/AKT/mTOR pathway.

Conclusion: With high expression in patients with GC, SNHG6 can promote the development of GC by activating the PI3K/AKT/mTOR signaling pathway and suppressing the autophagy of cells. Therefore, it is a potential breakthrough in the diagnosis and treatment of GC in the future.