The Pro-Apoptotic Activity of Tamarixetin on Liver Cancer Cells Via Regulation Mitochondrial Apoptotic Pathway

被引:0
作者
Jing Xu
Xinhao Cai
Shanshan Teng
Jiahui Lu
Yulin Zhou
Xiaofeng Wang
Zhaoli Meng
机构
[1] Jilin University,Cardiovascular Disease Center, First Hospital of Jilin University
[2] Jilin University,School of Life Sciences
[3] Jilin University,Department of Stomatology, China
[4] Jilin University,Japan Union Hospital of Jilin University
来源
Applied Biochemistry and Biotechnology | 2019年 / 189卷
关键词
Tamarixetin; Liver cancer; Apoptosis; Mitochondria; ERKs and AKT;
D O I
暂无
中图分类号
学科分类号
摘要
Based on the various pharmacological activities of tamarixetin, the present study investigated the cytotoxicity property of tamarixetin in human liver cancer cells including PLC/PRF/5 and HepG2 cells, and their xenografted tumor nude mice. In cells, tamarixetin incubation resulted in the suppression on cell viability; enhanced cell apoptosis rate, LDH release, caspase-3 activation, and reactive oxygen species accumulation; and decreased mitochondrial membrane potential in a dose-dependent manner. Tamarixetin inhibited the growth of PLC/PRF/5- and HepG2-xenografted tumors in BALB/c nude mice after 14-day administration without influencing their bodyweights and organ functions including liver and spleen. Tamarixetin enhanced the expression levels of pro-apoptotic proteins including Bax and cleaved caspase-3 and inhibited the expression levels of anti-apoptotic proteins including Bcl-2 and Bcl-xL in liver cancer cells and their xenografted tumor tissues. Furthermore, tamarixetin significantly suppressed the phosphorylation of ERKs and AKT in both PLC/PRF/5 and HepG2 cells, and tumor tissues. All present data suggest that tamarixetin displays pro-apoptotic properties in liver cancer cells related to the mitochondria apoptotic pathway via regulating the ERKs and AKT signaling.
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页码:647 / 660
页数:13
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