Chan Kun-Ming1, Cheng Chih-Hsien2, Lee Chen-Fang2, Wu Ting-Jung2, Chou Hong-Shiue2, Lee Wei-Chen2. 1. Department of General Surgery, Chang Gung Memorial Hospital at Linkou, Chang Gung University College of Medicine, Taoyuan, Taiwan. Electronic address: chankunming@adm.cgmh.org.tw. 2. Department of General Surgery, Chang Gung Memorial Hospital at Linkou, Chang Gung University College of Medicine, Taoyuan, Taiwan.
Abstract
BACKGROUND: Potential agents that can effectively treat hepatocellular carcinoma (HCC) are being continuously explored. METHODS: Celastrol extracted from roots of an ancient Chinese herb, Tripterygium wilfordii (Thunder god vine), has been identified as a potential anti-tumor agent. In this study, the molecular mechanisms underlying the action of celastrol on cell proliferation and chemokine CXCR4-related signal pathway associated with tumor growth were investigated. RESULTS: The CXCR4 expression was diminished by celastrol treatment in a dose-dependent manner, and its downstream associated pathways, including PI3K and Akt were also downregulated. Celastrol also significantly attenuated proliferation and migration ability of HCC cells, and induced cell apoptosis in vitro. Additionally, significant inhibition of HCC growth was observed in the celastrol-treated group as compared with the control group in vivo as well. CONCLUSION: Celastrol is capable of attenuating cell proliferation and inducing apoptosis, leading to inhibition of HCC growth through the suppression of CXCR4-related signal pathway.
BACKGROUND: Potential agents that can effectively treat hepatocellular carcinoma (HCC) are being continuously explored. METHODS:Celastrol extracted from roots of an ancient Chinese herb, Tripterygium wilfordii (Thunder god vine), has been identified as a potential anti-tumor agent. In this study, the molecular mechanisms underlying the action of celastrol on cell proliferation and chemokine CXCR4-related signal pathway associated with tumor growth were investigated. RESULTS: The CXCR4 expression was diminished by celastrol treatment in a dose-dependent manner, and its downstream associated pathways, including PI3K and Akt were also downregulated. Celastrol also significantly attenuated proliferation and migration ability of HCC cells, and induced cell apoptosis in vitro. Additionally, significant inhibition of HCC growth was observed in the celastrol-treated group as compared with the control group in vivo as well. CONCLUSION:Celastrol is capable of attenuating cell proliferation and inducing apoptosis, leading to inhibition of HCC growth through the suppression of CXCR4-related signal pathway.