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Ginsenoside compound K induces mitochondrial apoptosis in human hepatoma cells through Bclaf1-mediated modulation of ERK signaling.
- Source :
-
Food & Agricultural Immunology . Dec2022, Vol. 33 Issue 1, p799-816. 18p. - Publication Year :
- 2022
-
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. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 09540105
- Volume :
- 33
- Issue :
- 1
- Database :
- Academic Search Index
- Journal :
- Food & Agricultural Immunology
- Publication Type :
- Academic Journal
- Accession number :
- 160508497
- Full Text :
- https://doi.org/10.1080/09540105.2022.2134313