Background: Receptor-interacting protein (RIP) has been shown to play a critical role in the development of cancer cells. Nevertheless, its functional role in hepatocellular carcinoma (HCC) progression is not fully understood.
Methods: Western blotting and qRT-PCR were used to detect the expression level of RIP6 in clinical tissues of HCC and HCC cell lines; MTT methods, cells flow cytometry, plate cloning, and nude mice tumor formation were used to verify the effect of RIP6 on HCC progression in in vivo and in vitro experiments.
Results: Here, we first observed that RIP6 was significantly down-regulated in HCC tissue compared to adjacent normal tissues. In HCC patients, RIP6 low expression was positively related with tumor size. In addition, we found that RIP6 promoted HCC cell apoptosis to inhibit cancer progress. Further studies demonstrated RIP6 also suppressed HCC cell proliferation to further regulate cancer growth. Mechanistically, we demonstrated that RIP6 over-expression could lead to smaller tumor size in vivo.
Conclusions: RIP6 inhibited tumor cell growth by promoting cell apoptosis and suppressing cell proliferation of HCC in vivo and in vitro. Therefore, our studies provided the novel insight into the role of RIP6 in HCC progress and a potential new molecular target for treating HCC.