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Selenium and sulindac are synergistic to inhibit intestinal tumorigenesis in Apc/p21 mice

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Title: Selenium and sulindac are synergistic to inhibit intestinal tumorigenesis in Apc/p21 mice
Author(s): Bi, Xiuli; Pohl, Nicole; Dong, Huali; Yang, Wancai
Subject(s): Selenium Sulindac Cancer prevention
Abstract: Background: Both selenium and non-steroidal anti-inflammatory drug (NSAID) sulindac are effective in cancer prevention, but their effects are affected by several factors including epigenetic alterations and gene expression. The current study was designed to determine the effects of the combination of selenium and sulindac on tumor inhibition and the underlying mechanisms. Results: We fed the intestinal tumor model Apc/p21 mice with selenium- and sulindac-supplemented diet for 24 weeks, and found that the combination of selenium and sulindac significantly inhibited intestinal tumorigenesis, in terms of reducing tumor incidence by 52% and tumor multiplicities by 80% (p<0.01). Mechanistic studies revealed that the combination of selenium and sulindac led to the significant induction of the expression of p27 and p53 and JNK1 phosphorylation, and led to the suppression of β-catenin and its downstream targets. Impressively, the data also showed that demythelation on p21 promoter was associated with tumor inhibition by the combination of selenium and sulindac. Conclusions: The selenium is synergistic with sulindac to exert maximal effects on tumor inhibition. This finding provides an important chemopreventive strategy using combination of anti-cancer agents, which has a great impact on cancer prevention and has a promising translational potential.
Issue Date: 2013-01
Publisher: BioMed Central
Citation Info: Bi, X. L., Pohl, N., Dong, H. L. and Yang, W. C. Selenium and sulindac are synergistic to inhibit intestinal tumorigenesis in Apc/p21 mice. Journal of Hematology & Oncology. 2013. 6. DOI: 10.1186/1756-8722-6-8
Type: Article
Description: © 2013 Bi et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. © 2013 by BioMed Central, Journal of Hematology and Oncology
ISSN: 1756-8722
Sponsor: This work was supported in part by National Institutes of Health grant, USA (R01 CA112081 to W. Yang), the grants from the Nature Science Foundation of China (Grants 81272251 and 91229115 to W.Yang, Grants 81001003 and 81272333 to X. Bi) and the Program of Liaoning Excellent Talents in University (LETU #LJQ2011002 to X. Bi).
Date Available in INDIGO: 2013-12-02

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