miR-103 promotes hepatocellular carcinoma cell proliferation and migration in the simulation transition zone of RFA through PI3K/Akt signaling pathway by targeting PTEN.

Radiofrequency ablation (RFA) is a potentially curative therapy for nontransplantable hepatocellular carcinoma (HCC). However, as tumor size increases, incomplete RFA can increase rates of local recurrence and tumor progression. As such, there remains a need to identify potential biologic mechanisms mediating HCC response to thermal ablation. Our results revealed that miR-103 was markedly upregulated in recurrent HCC tissues treated with RFA as first-line treatment and in HCC lines after heat stress in vitro, simulating the marginal zone of RFA treatment. Gain-of-function and loss-of-function studies showed that miR-103 ectopic overexpression promoted, but miR-103 silencing reduced, heat-exposed HCC proliferation, and migration in vitro. Western blotting displayed that proteins related with proliferation and migration were significantly changed in different groups. Furthermore, PTEN may be a potential target of miR-103 and miR-103 could activate the PI3K/Akt pathway by suppressing PTEN expression. Taken together, these studies provide experimental evidence supporting a role for miR-103 in HCC response to heat stress.