METase promotes cell autophagy via promoting SNHG5 and suppressing miR-20a in gastric cancer.

Background: Gastric cancer (GC) severely threatens human life, and METase seemed to inhibit tumor growth. However, the potential mechanism underlying it is still unclear.

Methods: Both clinical tissues and cell lines were used in the present study. SNHG5 and miR-20a expressions were determined using real-time PCR. Western blot was performed to determine the expression of autophagy-related proteins. The interaction between miR-20a and SNHG5 was determined using luciferase reporter assay and RNA immunoprecipitation (RIP).

Results: The expression of SNHG5 was decreased in GC tissues and cell lines. Overexpressed METase significantly promoted cell apoptosis and autophagy, as well as the expression of SNHG5. SNHG5 directly regulated the expression of miR-20a. GC cells transfected with pcDNA-SNHG5 significantly promoted cell apoptosis and autophagy, while the co-transfected with miR-20a mimic dramatically reversed the effects of pcDNA-SNHG5. Overexpressed METase significantly promoted cell autophagy, which was abolished by down-regulated SNHG5.

Conclusion: Overexpressed METase promoted cell apoptosis and autophagy via up-regulating the expression of SNHG5 and down-regulating miR-20a in GC.