Microbiota as a mediator of cancer progression and therapy

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• 作者：Jillian L. Pope^a ; Sarah Tomkovich^a ; ^b ; Ye Yang^a ; Christian Jobin^a ; ^c ; ^{christian.jobin@medicine.ufl.edu}
• 关键词：AOM ; azoxymethane ; Apc ; adenomatous polyposis coli ; CAC ; colitis associated cancer ; CRC ; colorectal cancer ; DNA-PK ; DNA-dependent protein kinase ; GF ; germ free ; GI ; gastrointestinal ; IBD ; inflammatory bowel diseases ; IL ; interleukin ; MAIT ; mucosa-associated invariant T ; MTX ; methotrexate ; NLR ; NOD-like receptor ; NLRP1 ; NLR family ; pyrin domain containing 1 ; NOD ; nucleotide-binding oligomerization domain-containing protein ; PDL-1 ; programmed cell death protein 1 ligand 1 ; PI3K ; phosphoinositide 3
• 刊名：Translational Research
• 出版年：2017
• 出版时间：January 2017
• 年：2017
• 卷：179
• 期：Complete
• 页码：139-154
• 全文大小：706 K
• 卷排序：179

文摘

Complex and intricate circuitries regulate cellular proliferation, survival, and growth, and alterations of this network through genetic and epigenetic events result in aberrant cellular behaviors, often leading to carcinogenesis. Although specific germline mutations have been recognized as cancer inducers, the vast majority of neoplastic changes in humans occur through environmental exposure, lifestyle, and diet. An emerging concept in cancer biology implicates the microbiota as a powerful environmental factor modulating the carcinogenic process. For example, the intestinal microbiota influences cancer development or therapeutic responses through specific activities (immune responses, metabolites, microbial structures, and toxins). The numerous effects of microbiota on carcinogenesis, ranging from promoting, preventing, or even influencing therapeutic outcomes, highlight the complex relationship between the biota and the host. In this review, we discuss the latest findings on this complex microbial interaction with the host and highlight potential mechanisms by which the microbiota mediates such a wide impact on carcinogenesis.