Ruxi Lv1, Min Zhu2, Kun Chen3, Haitao Xie4, Hongxia Bai1, Qingfa Chen5. 1. Department of Gastroenterology, Liaocheng People's Hospital, Liaocheng 252000, China. 2. Clinical Laboratory, Liaocheng People's Hospital, Liaocheng 252000, China. 3. College of Medicine, Liaocheng University, Liaocheng 252000, China. 4. Centre for Research, Xiankangda Bio-Tech Corporation, Dongguan 523000, China. 5. The Institute for Tissue Engineering and Regenerative Medicine, The Liaocheng University/Liaocheng People's Hospital, Liaocheng 252000, China.
Abstract
BACKGROUND: To study the effects of z-guggulsterone on gastric cancer cell apoptosis and the mechanism related. MATERIALS AND METHODS: Human gastric tumor SGC-7901 cells and GES-1 normal epithelial cells were treated with z-guggulsterone (0-75 μM) for 24 h. MTT assay was applied to evaluate cell proliferation. Flow cytometry and Hoechst staining were used to assess cell apoptosis. Western blotting was applied to evaluate FXR, small heterodimer partner (SHP), Bcl-2, and Bax protein expression. ELISA was applied to gain the levels of active caspase-3 and the contents of TNF-α, TGF-β1, and VEGF. RESULTS: The expression levels of FXR and SHP were higher in tumor cells than in normal epithelial cells. Inhibition of FXR signaling with z-guggulsterone dose-dependently inhibited SGC-7901 cell proliferation and promoted SGC-7901 cell apoptosis. Bcl-2 protein expression was significantly decreased, and active caspase-3 and Bax protein expression was increased in SGC-7901 cells incubated with z-guggulsterone. The content of TNF-α was significantly increased, and the contents of VEGF and TGF-β1 were decreased in SGC-7901 cells incubated with z-guggulsterone. CONCLUSIONS: Inhibition of FXR signaling with z-guggulsterone induced anticancer effects in SGC-7901 cells by decreasing cell proliferation and promoting apoptosis. Z-guggulsterone induced cell apoptosis through the mitochondria-dependent pathway.
BACKGROUND: To study the effects of z-guggulsterone on gastric cancer cell apoptosis and the mechanism related. MATERIALS AND METHODS: Human gastric tumor SGC-7901 cells and GES-1 normal epithelial cells were treated with z-guggulsterone (0-75 μM) for 24 h. MTT assay was applied to evaluate cell proliferation. Flow cytometry and Hoechst staining were used to assess cell apoptosis. Western blotting was applied to evaluate FXR, small heterodimer partner (SHP), Bcl-2, and Bax protein expression. ELISA was applied to gain the levels of active caspase-3 and the contents of TNF-α, TGF-β1, and VEGF. RESULTS: The expression levels of FXR and SHP were higher in tumor cells than in normal epithelial cells. Inhibition of FXR signaling with z-guggulsterone dose-dependently inhibited SGC-7901 cell proliferation and promoted SGC-7901 cell apoptosis. Bcl-2 protein expression was significantly decreased, and active caspase-3 and Bax protein expression was increased in SGC-7901 cells incubated with z-guggulsterone. The content of TNF-α was significantly increased, and the contents of VEGF and TGF-β1 were decreased in SGC-7901 cells incubated with z-guggulsterone. CONCLUSIONS: Inhibition of FXR signaling with z-guggulsterone induced anticancer effects in SGC-7901 cells by decreasing cell proliferation and promoting apoptosis. Z-guggulsterone induced cell apoptosis through the mitochondria-dependent pathway.
Authors: Eun Soo Kim; Sung Yi Hong; Hye Kyung Lee; Seung Won Kim; Min Ji An; Tae Il Kim; Kyoung Ryul Lee; Won Ho Kim; Jae Hee Cheon Journal: Oncol Rep Date: 2008-12 Impact factor: 3.906