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Publication Detail

Title: Hydrogen peroxide/ATR-Chk2 activation mediates p53 protein stabilization and anti-cancer activity of cheliensisin A in human cancer cells.

Authors: Zhang, Jingjie; Gao, Guangxun; Chen, Liang; Li, Jingxia; Deng, Xu; Zhao, Qin-shi; Huang, Chuanshu

Published In Oncotarget, (2014 Feb 15)

Abstract: Chiliensisine A (Chel A) as a novel styryl-lactone isolated from Goniothalamus cheliensis Hu has been indicated to be a chemotherapeutic agent in Leukemia HL-60 cells. However, its potential for cancer treatment and the underlying mechanisms are not deeply investigated to the best of our knowledge. Current studies showed that Chel A could trigger p53-mediated apoptosis, accompanied with dramatically inhibition of anchorage-independent growth of human colon cancer HCT116 cells. Further studies found that Chel A treatment resulted in p53 protein stabilization and accumulation via the induction of its phosphorylation at Ser20 and Ser15. Moreover, Chel A-induced p53 protein accumulation and activation required ATR/Chk2 axis, which is distinct from the mechanism that we have most recently identified the Chk1/p53-dependent apoptotic response by Chel A in normal mouse epidermal Cl41 cells. In addition, our results demonstrated that hydrogen peroxide generation induced by Chel A acted as a precursor for all these signaling events and downstream biological effects. Taken together, we have identified the Chel A as a new therapeutic agent, which highlights its potential for cancer therapeutic effect.

PubMed ID: 24553354 Exiting the NIEHS site

MeSH Terms: Apoptosis/drug effects; Ataxia Telangiectasia Mutated Proteins/genetics; Ataxia Telangiectasia Mutated Proteins/metabolism; Checkpoint Kinase 2/genetics; Checkpoint Kinase 2/metabolism*; Colonic Neoplasms/drug therapy*; Colonic Neoplasms/metabolism; Colonic Neoplasms/pathology; Epoxy Compounds/pharmacology*; HCT116 Cells; Humans; Hydrogen Peroxide/metabolism*; Pyrones/pharmacology*; Signal Transduction; Transfection; Tumor Suppressor Protein p53/genetics; Tumor Suppressor Protein p53/metabolism*; Tumor Suppressor Proteins/genetics; Tumor Suppressor Proteins/metabolism

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