p53 mutations in colorectal cancer- molecular pathogenesis and pharmacological reactivation (original) (raw)

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Copyright ©The Author(s) 2015. Published by Baishideng Publishing Group Inc. All rights reserved.

World J Gastroenterol. Jan 7, 2015; 21(1): 84-93
Published online Jan 7, 2015. doi: 10.3748/wjg.v21.i1.84

Figure 3 Small molecule compounds pharmacologically reactivating of p53 function. MI43 and Nutlin-3 bound to MDM2 blocking MDM2-p53 interaction. RITA bound to p53 interfering MDM2-p53 interaction. α-Lipoic acid increased p53 protein stability and its apoptotic effect. Quinacrine induced the autophagy-associated cell death in a p53-dependent manner. NSC17632 activated p53-like activatity dependent on p73. PRIMA-1/PRIMA-1MET restored mutant p53 to exert apoptotic effect. Maslinic acid and Epicatechin gallate as plant extraction modulated the expression of p53 and its target genes in p53-dependent apoptotic and cell cycle arrest pathway.

• Citation: Li XL, Zhou J, Chen ZR, Chng WJ. p53 mutations in colorectal cancer- molecular pathogenesis and pharmacological reactivation. World J Gastroenterol 2015; 21(1): 84-93
• URL: https://www.wjgnet.com/1007-9327/full/v21/i1/84.htm
• DOI: https://dx.doi.org/10.3748/wjg.v21.i1.84