Published online Dec 21, 2015. doi: 10.3748/wjg.v21.i47.13277
Peer-review started: May 8, 2015
First decision: July 19, 2015
Revised: August 24, 2015
Accepted: October 17, 2015
Article in press: October 20, 2015
Published online: December 21, 2015
Processing time: 230 Days and 3.8 Hours
AIM: To investigate the effects of guggulsterone on the proliferation and apoptosis of human hepatoma HepG2 cells in vitro and relevant mechanisms.
METHODS: Human hepatocellular carcinoma HepG2 cells and normal human liver L-02 cells were treated with different concentrations of guggulsterone (5-100 μmol/L) for 24-72 h. Cell proliferation was tested by MTT assay. Cell cycle and apoptosis were investigated using flow cytometry (FACS). Bcl-2 and Bax mRNA and protein expression was detected by real-time PCR and Western blot, respectively. TGF-β1, TNF-α, and VEGF contents were determined by ELISA.
RESULTS: Guggulsterone significantly inhibited HepG2 cell proliferation in a dose- and time-dependent manner. FACS showed that guggulsterone arrested HepG2 cell cycle at G0/G1 phase. Guggulsterone induced apoptosis was also observed in HepG2 cells, with 24.91% ± 2.41% and 53.03% ± 2.28% of apoptotic cells in response to the treatment with 50 μmol/L and 75 μmol/L guggulsterone, respectively. Bax mRNA and protein expression was significantly increased and Bcl-2 mRNA and protein expression was decreased. ELISA analysis showed that the concentrations of TGF-β1 and VEGF were significantly decreased and TNF-α concentration was increased.
CONCLUSION: Guggulsterone exerts its anticancer effects by inhibiting cell proliferation and inducing apoptosis in HepG2 cells. Guggulsterone induces apoptosis by activation of the intrinsic mitochondrial pathway.
Core tip: Hepatocellular carcinoma (HCC) is the fifth most prevalent cancer and the second leading cause of tumor mortality worldwide. Guggulsterone (GS) is a phytosterol extracted from the gum resin of guggul plants, and its pro-apoptotic effect has been found to play a pivotal role in its anti-carcinogenic mechanisms. In this study, we investigated the anticancer effects of GS-induced apoptosis in human HCC cells and the underlying molecular mechanisms. Our results demonstrated that GS induced HepG2 cell apoptosis through regulating Bcl-2 and Bax expression levels.