Microbiota impact on the epigenetic regulation of colorectal cancer

被引:78
|
作者
Yang, Tao [1 ,2 ]
Owen, Jennifer L. [1 ,2 ]
Lightfoot, Yaima L. [1 ,2 ]
Kladde, Michael P. [3 ]
Mohamadzadeh, Mansour [1 ,2 ]
机构
[1] Univ Florida, Dept Infect Dis & Pathol, Gainesville, FL 32608 USA
[2] Univ Florida, Dept Med, Div Gastroenterol Hepatol & Nutr, Gainesville, FL 32610 USA
[3] Univ Florida, Dept Biochem & Mol Biol, Gainesville, FL 32610 USA
基金
美国国家卫生研究院;
关键词
colorectal cancer; commensal bacteria; epigenetic regulation; inflammatory bowel disease; microbiota; LACTOBACILLUS-ACIDOPHILUS DEFICIENT; ISLAND METHYLATOR PHENOTYPE; RUNX3 PROMOTER METHYLATION; MYC PROTEIN DISTRIBUTION; KAPPA-B ACTIVATION; GENE-EXPRESSION; GUT MICROBIOTA; MICROSATELLITE INSTABILITY; INTESTINAL INFLAMMATION; ULCERATIVE-COLITIS;
D O I
10.1016/j.molmed.2013.08.005
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Mechanisms of colorectal cancer (CRC) development can be generally divided into three categories: genetic, epigenetic, and aberrant immunologic signaling pathways, all of which may be triggered by an imbalanced intestinal microbiota. Aberrant gut microbial composition, termed 'dysbiosis', has been reported in inflammatory bowel disease patients who are at increased risk for CRC development. Recent studies indicate that it is feasible to rescue experimental models of colonic cancer by oral treatment with genetically engineered beneficial bacteria and/or their immune-regulating gene products. Here, we review the mechanisms of epigenetic modulation implicated in the development and progression of CRC, which may be the result of dysbiosis, and therefore may be amenable to therapeutic intervention.
引用
收藏
页码:714 / 725
页数:12
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