[Knockdown of B7-H4/VTCN1 promotes apoptosis and autophagy of Huh7 cells by inhibiting phosphorylation of JNK].

Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi

Department of Hepatobiliary Surgery, First Affiliated Hospital, Chongqing Medical University, Chongqing 400016, China. *Corresponding author, E-mail:

Published: July 2020

Objective To investigate the effects of co-stimulatory molecule B7-H4/VTCN1 on apoptosis and autophagy of hepatocellular carcinoma (HCC) cells and the potential signaling pathways. Methods After Huh7 cells were treated by B7-H4 siRNA, CCK-8 assay was used to detect the cell proliferation. Cell apoptosis was measured by flow cytometry. The protein expression levels of cleaved caspase-3 (c-caspase-3), Bcl2, LC3, P62, JNK and phosphorylated JNK (p-JNK) were examined by Western blot analysis. The autophagosome was observed by monodansylcadaverine (MDC) assay. Results After the knockdown of B7-H4, the apoptosis and autophagy of HCC cells increased, and cell proliferation decreased. Moreover, the expression levels of c-caspase-3 and LC3 II went up, while the expression levels of Bcl2 and P62 went down. Furthermore, the phosphorylation of JNK was also inhibited, and autophagosome was visible. Conclusion Knockdown of B7-H4 promotes the apoptosis and autophagy in HCC cells, which may be related to the inhibited phosphorylation of JNK.

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