Author: Dong, Xiaoxv; Ni, Boran; Fu, Jing; Yin, Xingbin; You, Longtai; Leng, Xin; Liang, Xiao; Ni, Jian
Title: Emodin induces apoptosis in human hepatocellular carcinoma HepaRG cells via the mitochondrial caspase-dependent pathway Document date: 2018_8_2
ID: 02r8i5n1_29
Snippet: Apoptosis initiated by increased ROS production after emodin treatment might induce apoptosis-related protein change. Compared with the control cells, our data suggested that the treatment of HepaRG cells with emodin significantly increased the protein expression levels of p53, p21, Bax, cleaved caspases-3, and -9 and PARP, while emodin decreased Bcl-2 levels. Furthermore, emodin promoted cytochrome c release from mitochondria into the cytosol. P.....
Document: Apoptosis initiated by increased ROS production after emodin treatment might induce apoptosis-related protein change. Compared with the control cells, our data suggested that the treatment of HepaRG cells with emodin significantly increased the protein expression levels of p53, p21, Bax, cleaved caspases-3, and -9 and PARP, while emodin decreased Bcl-2 levels. Furthermore, emodin promoted cytochrome c release from mitochondria into the cytosol. Previous studies have shown that emodin induced apoptosis in cancer cells through the mitochondrial-dependent apoptotic pathway (47) (48) (49) , which was consistent with our experiments. In addition, emodin induced hepatocellular carcinoma cell apoptosis through the mitogen-activated protein kinase (MAPK) and phosphoinositide 3-kinase (PI3K)/AKT signaling pathways (15, 50) .
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