Abstract
Emodin, a natural anthraquinone isolated from the traditional Chinese medicine Radix rhizoma Rhei, can induce apoptosis in many kinds of cancer cells. This study demonstrated that emodin induces apoptosis in human colon cancer HCT116 cells by provoking oxidative stress, which subsequently triggers a p53-mitochondrial apoptotic pathway. Emodin induced mitochondrial transmembrane potential loss, increase in Bax and decrease in Bcl-2 expression and mitochondrial translocation and release of cytochrome c to cytosol in HCT116 cells. In response to emodin-treatment, ROS increased rapidly, and subsequently p53 was overexpressed. Pretreatment with the antioxidant NAC diminished apoptosis and p53 overexpression induced by emodin. Transfecting p53 siRNA also attenuated apoptosis induced by emodin, Bax expression and mitochondrial translocation being reduced compared to treatment with emodin alone. Taken together, these results indicate that ROS is a trigger of emodin-induced apoptosis in HCT116 cells, and p53 expression increases under oxidative stress, leading to Bax-mediated mitochondrial apoptosis.
Highlights
Colorectal cancer is one of the most common cancers globally
This study demonstrated that emodin induces apoptosis in human colon cancer HCT116 cells by provoking oxidative stress, which subsequently triggers a p53-mitochondrial apoptotic pathway
We explored the change of ROS level in the emodin-induced HCT116 cells
Summary
Colorectal cancer is one of the most common cancers globally. In 2012, the worldwide incidence number was estimated to be 1,361,000, the third most next to lung and breast cancer. Almost 55% of the cases occur in more developed regions, but the mortality was higher in less developed regions (52.02%) that in more developed regions (47.98%) (International Agency for Research on Cancer, 2014a). In China, along with the changes in diet and life style, the ASR (age-standardised rate) of incidence and mortality has increased to 14.2 and 7.4 per 100,000 respectively(International Agency for Research on Cancer, 2014b). It has been demonstrated that emodin suppresses tumor growth in tumor nude mice xenografts bearing human colon cancer LS1034 cells and induce LS1034 cells apoptosis in vitro (Ma et al, 2012). Emodin could inhibit VEGF-receptor phosphorylation in human colon cancer HCT116 cells (Lu et al, 2008). The molecular mechanisms of emodin-induced apoptosis in colorectal cancer cells need more investigation
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