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ABSTRACT
Compound K (CK) is the metabolite and final active ingredient of diol-type ginsenosides. In this study, we investigated the effect of CK on mitochondrial apoptosis in SMMC-7721 and BEL-7404 cells and the regulatory mechanism through in vitro and in vivo experiments. The results demonstrated that CK inhibited Hepatocellular carcinoma (HCC) cells proliferation and arrested the cells in G0/G1 phase. CK induces mitochondrial apoptosis in HCC cells and inhibited p-ERK expression. Bcl-2 associated transcription factor 1 (Bclaf1) was distributed in the nucleus and cytoplasm, and CK inhibited its expression. Treatment of a nude mouse xenograft model bearing SMMC-7721 cells with CK decreased the expression of Bclaf1, p-ERK, and Bcl-2 but increased that of Bax. In summary, ginsenoside CK downregulated Bclaf1 expression, inhibited the activation of the ERK pathway, and triggered mitochondrial apoptosis in HCC. These findings uncovered a potential therapeutic strategy leveraging the anti-tumor effects of CK against HCC.
Acknowledgements
XZ and JC designed the study; JC and MS performed the research, analyzed data, and wrote the initial draft of the paper; XC contributed to refining the ideas, carrying out additional analyses and finalizing this paper.
Disclosure statement
No potential conflict of interest was reported by the author(s).
Data availability statement
All data underlying this study are presented in the article. Further inquiries can be directed to the corresponding author.
Ethics statement
The experiment procedures were approved by the Institutional Animal Care and Use Committee of Yanbian University (Resolution number, 201501022).