Vitexin suppresses autophagy to induce apoptosis in hepatocellular carcinoma via activation of the JNK signaling pathway

• DOI: 10.18632/oncotarget.11731
• Publication Date: 2016-08-31T17:50:10Z
• Authors: Jin-Dan He; Zhen Wang; Shi-Peng Li; Yan-Jie Xu; Yao Yu; Yi-Jie Ding; Wen-Li Yu; Rong-Xin Zhang; Hai-Ming Zhang; Hong-Yin Du
• Keywords: Viability assay

// Jin-Dan He 1, * , Zhen Wang Shi-Peng Li 4, Yan-Jie Xu Yao Yu 1 Yi-Jie Ding Wen-Li 2 Rong-Xin Zhang 5 Hai-Ming 3 Hong-Yin Du 2, First Central Clinical College, Tianjin Medical University, 300192, P.R. China Department of Anesthesiology, Hospital, Liver Transplantation, Oriental Organ Transplant Center Key Laboratory Transplantation Tianjin, 4 General Surgery, The People's Hospital Jiaozuo City, 454002, Immunology and Inflammation, Immunology, Immune Microenvironment Diseases Educational Ministry China, Basic 300070, These authors have contributed equally to this work Correspondence to: Du, email: [e-mail] Zhang, [e-mail] Keywords: vitexin, hepatocellular carcinoma, autophagy, apoptosis, JNK signaling Received: June 15, 2016 Accepted: August Published: 31, ABSTRACT Vitexin, a flavonoids compound, is known exhibit broad anti-oxidative, anti-inflammatory, analgesic, antitumor activity in many cancer xenograft models cell lines. purpose study was investigate the effects underlying mechanisms vitexin on carcinoma. In study, we found that suppressed viability HCC lines (SK-Hep1 Hepa1-6 cells) significantly. Vitexin showed cytotoxic against vitro by inducing apoptosis inhibiting autophagy. induced concentration-dependent manner, caused up-regulations Caspase-3, Cleave down-regulation Bcl-2. expression autophagy-related protein LC3 II significantly decreased after treatment. Moreover, western blot analysis presented markedly up-regulated levels p-JNK down-regulated p-Erk1/2 SK-Hep1 cells cells. Cotreatment with inhibitor SP600125, demonstrated suppressed, while inhibition autophagy reversed. results colony formation assay mouse model confirmed growth role vivo . conclusion, inhibits way induction suppression, both which are through MAPK pathway. Therefore, could be regarded as potent therapeutic agent for treatment HCC.