LncRNA SNHG3 promotes the progression of cholangiocarcinoma by regulating miR-151a-3p/STAT5a axis

Abstract Background Cholangiocarcinoma (CCA) is a highly aggressive malignant adenoma. LncRNA SNHG3 was reported to be a prognostic biomarker for CCA. The aim of this study was to explore the function and potential mechanisms of SNHG3 in CCA. Methods and Results Clinical CCA samples were collected to detect SNHG3, miR-151a-3p, and STAT5a levels, and their correlation was evaluated by Pearson correlation analysis. IHC was used to assess STAT5a expression. CCK-8, TUNEL, wound healing, and transwell assays were used to identify cell viability, apoptosis, migration, and invasion. Dual-luciferase reporter experiment was conducted to verify the relation between SNHG3 and miR-151a-3p, STAT5a and miR-151a-3p.. SNHG3 and STAT5a levels were significantly up-regulated in CCA tissues and cells, while miR-151a-3p level was down-regulated in CCA tissues and cells. Inhibition of SNHG3 suppressed CCA cell proliferation, apoptosis, migration and invasion. Mechanically, SNHG3 directly targeted miR-151a-3p in CCA, and miR-151a-3p inhibitor reversed the inhibitory roles of inhibition of SNHG3 on the aggressive behaviors of HUCC-T1 cells. Furthermore, STAT5a was identified as a potential target of miR-151a-3p. Functionally, inhibition of STAT5a reversed the roles of inhibition of SNHG3 and miR-151a-3p on CCA cells aggressive behaviors. Conclusion SNHG3 promoted the progression of CCA by regulating miR-151a-3p/STAT5a axis, which provided a promising target for CCA treatment.