GAS6-AS2 Promotes Hepatocellular Carcinoma via miR-3619-5p/ARL2 Axis Under Insufficient Radiofrequency Ablation Condition.

Abstract

Background: Hepatocellular carcinoma (HCC) is a common malignancy worldwide. Radiofrequency ablation (RFA) is applied for treating HCC; however, insufficient RFA promotes HCC development and accelerates HCC recurrence. Therefore, the molecular functions underlying this process have gradually attracted attention. Objective: We sought to examine whether GAS6-AS2 (also known as GAS6-DT: growth arrest specific 6 divergent transcript) played a role in the development of HCC after insufficient RFA. Materials and Methods: The in vitro model was established by heating Huh7 and MHCC97 cells in water bath at 47°C, named as Huh7-H and MHCC97-H. Colony formation, transwell and Western blot assays were conducted for functional analysis. Results: GAS6-AS2 was upregulated in Huh7-H and MHCC97-H cells relative to Huh7 and MHCC97 cells. GAS6-AS2 deficiency hampered cell proliferation, migration, invasion, epithelial-mesenchymal transition, and stemness in Huh7-H and MHCC97-H cells. Moreover, microRNA-3619-5p (miR-3619-5p) combined with GAS6-AS2 and ARL2 (ADP ribosylation factor-like GTPase 2) was the target gene of miR-3619-5p. GAS6-AS2 served as the competing endogenous RNA (ceRNA) of ARL2 via absorbing miR-3619-5p. Conclusion: On the whole, present study uncovered a novel ceRNA mechanism of GAS6-AS2/miR-3619-5p/ARL2 in HCC after insufficient RFA, which might shed a new insight into treatment of HCC after insufficient RFA.