科研之友
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摘要
Aloin has the potential to be a novel anticancer agent in cancer therapies. However, the detailed anticancer effect of Aloin remains to be fully elucidated. The present study analyzed the p53-dependent mechanisms in response to Aloin treatment. Using the p53-proficient A549 cells, an Aloin-induced apoptotic cell model was established, which was used to evaluate the potential underlying molecular mechanisms. The results demonstrated that 200, 300 and 400 mu M Aloin induced intrinsic cell apoptosis, which was further confirmed by disruption of the mitochondrial membrane potential, elevation of cytosolic Ca2+ levels, and activation of B-cell lymphoma 2 (Bcl-2) homologous antagonist killer, Bcl-2 X-associated protein, p53 upregulated modulator of apoptosis and phorbol-12-myristate-13-acetate-induced protein 1. Aloin-induced apoptosis was also accompanied by the induction of p53 phosphorylation on Serine (Ser) 15, Threonine 18, Ser20 and Ser392; however, there were no significant differences in the expression of p53 and mouse double minute 2 homolog. Aloin-induced apoptosis was reactive oxygen species (ROS) -and c-Jun/p38-dependent, as specific inhibitors for ROS, phosphorylated (p) -c-Jun and p-p38 may attenuate Aloin-induced A549 cell proliferating inhibition. In conclusion, these results suggested that Aloin may induce apoptosis in A549 cells via the ROS-mitogen activated protein kinase signaling pathway, with p53 phosphorylation. These results implicate Aloin as a potential therapeutic agent for the treatment of lung cancer.
- 出版日期2017-11
- 单位华中科技大学
