Progress in the study of imbalance of intestinal flora and the risk of colorectal cancer

doi:10.3877/cma.j.issn.2095-3224.2021.01.015

Abstract

Abstract:

Colorectal cancer (CRC) is one of the most common malignancies. The cause of its development and progression is unknown, a number of studies have concluded that lifestyle, diet, genetic and environmental factors all play a role. Intestinal flora maintains a dynamic balance under physiological conditions. When this balance is disturbed, the whole microecosystem will undergo major changes, and various intestinal flora and their metabolites can directly or indirectly promote the occurrence and development of colorectal cancer. In addition, diet, as an environmental factor, has an important effect on the composition and function of intestinal flora. The fiber and protein content in the diet is the main reason, and its influence is mainly mediated by microbial metabolites. In this review, we will summarize the research progress on the imbalance of intestinal flora and the risk of colorectal cancer from three perspectives: the mechanism of colorectal cancer, the metabolic effect of intestinal flora, and dietary intervention.

Key words: Diet, Colorectal neoplasms, Probiotics, Intestinal flora, Research progress

Chengzhang Zhu, Weisheng Zhang, Binbin Du, Xinlong Shi, He Wang, Zhipeng Liu, Jingjing Li, Xiongfei Yang. Progress in the study of imbalance of intestinal flora and the risk of colorectal cancer[J]. Chinese Journal of Colorectal Diseases(Electronic Edition), 2021, 10(01): 95-98.

/ / Recommend

Add to citation manager EndNote|Ris|BibTeX

URL: https://zhjzcjbdzzz.cma-cmc.com.cn/EN/10.3877/cma.j.issn.2095-3224.2021.01.015

https://zhjzcjbdzzz.cma-cmc.com.cn/EN/Y2021/V10/I01/95

References 47

[2]	Lin L, Zhang J. Role of intestinal microbiota and metabolites on gut homeostasis and human diseases [J]. BMC Immunol, 2017, 18(1): 2.
[3]	Xu Z, Knight R. Dietary effects on human gut microbiome diversity [J]. Br J Nutr, 2015, 113 Suppl(Suppl0): S1-S5.
[4]	Liang Q, Chiu J, Chen Y, et al. Fecal bacteria act as novel biomarkers for noninvasive diagnosis of colorectal cancer [J]. Clin Cancer Res, 2017, 23(8): 2061-2070.
[5]	Yang J, Yu J. The association of diet, gut microbiota and colorectal cancer: what we eat may imply what we get [J]. Protein Cell, 2018, 9(5): 474-487.
[6]	O'Keefe SJ. Diet, microorganisms and their metabolites, and colon cancer [J]. Nat Rev Gastroenterol Hepatol, 2016, 13(12): 691-706.
[7]	Tjalsma H, Boleij A, Marchesi JR, et al. A bacterial driver-passenger model for colorectal cancer: beyond the usual suspects [J]. Nat Rev Microbiol, 2012, 10(8): 575-582. URL
[8]	Beyer-Sehlmeyer G, Glei M, Hartmann E, et al. Butyrate is only one of several growth inhibitors produced during gut flora-mediated fermentation of dietary fibre sources [J]. Br J Nutr, 2003, 90(6): 1057-1070.
[9]	Zeng MY, Inohara N, Nuñez G. Mechanisms of inflammation-driven bacterial dysbiosis in the gut [J]. Mucosal Immunol, 2017, 10(1): 18-26.
[10]	赵日升，曹蕾，于君. 无菌鼠模型在结直肠癌研究中的应用 [J]. 中国实验动物学报, 2017, 25(6): 658-662.
[11]	Ding C, Tang W, Fan X, et al. Intestinal microbiota: a novel perspective in colorectal cancer biotherapeutics [J]. Onco Targets Ther, 2018, 11: 4797-4810.
[12]	Zeng MY, Inohara N, Nuñez G. Mechanisms of inflammation-driven bacterial dysbiosis in the gut [J]. Mucosal Immunol, 2017, 10(1): 18-26.
[13]	Zackular JP, Baxter NT, Chen GY, et al. Manipulation of the gut microbiota reveals role in colon tumorigenesis [J]. mSphere, 2015, 1(1): e00001-15.
[14]	Zackular JP, Baxter NT, Iverson KD, et al. The gut microbiome modulates colon tumorigenesis [J]. mBio, 2013, 4(6): e00692-13.
[15]	Pickard JM, Zeng MY, Caruso R, et al. Gut microbiota: Role in pathogen colonization, immune responses, and inflammatory disease [J]. Immunol Rev, 2017, 279(1): 70-89.
[16]	Han S, Gao J, Zhou Q, et al. Role of intestinal flora in colorectal cancer from the metabolite perspective: a systematic review [J]. Cancer Manag Res, 2018, 10: 199-206.
[17]	Romani L, Zelante T, Palmieri M, et al. The cross-talk between opportunistic fungi and the mammalian host via microbiota's metabolism [J]. Semin Immunopathol, 2015, 37(2): 163-171.
[18]	杨佳，于君. 饮食、肠道微生态与结直肠癌 [J/CD]. 中华结直肠疾病电子杂志, 2019, 8(6): 541-545.
[19]	Ribel-Madsen A, Ribel-Madsen R, Brøns C, et al. Plasma acylcarnitine profiling indicates increased fatty acid oxidation relative to tricarboxylic acid cycle capacity in young, healthy low birth weight men [J]. Physiol Rep, 2016, 4(19): e12977.
[20]	Kim MH, Kang SG, Park JH, et al. Short-chain fatty acids activate GPR41 and GPR43 on intestinal epithelial cells to promote inflammatory responses in mice [J]. Gastroenterology, 2013, 145(2): 396-406. URL
[21]	Bindels LB, Porporato P, Dewulf EM, et al. Gut microbiota-derived propionate reduces cancer cell proliferation in the liver [J]. Br J Cancer, 2012, 107(8): 1337-1344.
[22]	Lewis K, Lutgendorff F, Phan V, et al. Enhanced translocation of bacteria across metabolically stressed epithelia is reduced by butyrate [J]. Inflamm Bowel Dis, 2010, 16(7): 1138-1148.
[23]	Peng L, Li ZR, Green RS, et al. Butyrate enhances the intestinal barrier by facilitating tight junction assembly via activation of AMP-activated protein kinase in Caco-2 cell monolayers [J]. J Nutr, 2009, 139(9): 1619-1625.
[24]	Furusawa Y, Obata Y, Fukuda S, et al. Commensal microbe-derived butyrate induces the differentiation of colonic regulatory T cells [J]. Nature, 2013, 504(7480): 446-450. URL
[25]	Ryan M, Kochunov P, Rowland LM, et al. Lipid Metabolism, Abdominal Adiposity, and Cerebral Health in the Amish [J]. Obesity (Silver Spring), 2017, 25(11): 1876-1880.
[26]	Giang TM, Gaucel S, Brestaz P, et al. Dynamic modeling of in vitro lipid digestion: individual fatty acid release and bioaccessibility kinetics [J]. Food Chem, 2016, 194: 1180-1188.
[27]	Shen C, Xue M, Qiu H, et al. Insertion of neurotransmitters into a lipid bilayer membrane and its implication on membrane stability: a molecular dynamics study [J]. Chemphyschem, 2017, 18(6): 626-633.
[28]	Ridlon JM, Wolf PG, Gaskins HR. Taurocholic acid metabolism by gut microbes and colon cancer [J].Gut Microbes, 2016, 7(3): 201-215.
[29]	Savari S, Vinnakota K, Zhang Y, et al. Cysteinyl leukotrienes and their receptors: bridging inflammation and colorectal cancer [J].World J Gastroenterol, 2014, 20(4): 968-977.
[30]	Wang D, DuBois RN. An inflammatory mediator, prostaglandin E2, in colorectal cancer [J].Cancer J, 2013, 19(6): 502-510. URL
[31]	Kai M, Yamamoto E, Sato A, et al. Epigenetic silencing of diacylglycerol kinase gamma in colorectal cancer [J].Mol Carcinog, 2017, 56(7): 1743-1752.
[32]	Ma N, Tian Y, Wu Y, et al. Contributions of the Interaction Between Dietary Protein and Gut Microbiota to Intestinal Health [J].Curr Protein Pept Sci, 2017, 18(8): 795-808.
[33]	Espejo-Herrera N, Gràcia-Lavedan E, Boldo E, et al. Colorectal cancer risk and nitrate exposure through drinking water and diet [J].Int J Cancer, 2016, 139(2): 334-346.
[1]	Leystra AA, Clapper ML. Gut microbiota influences experimental outcomes in mouse models of colorectal cancer [J]. Genes (Basel), 2019, 10(11): 900.
[34]	Bingham SA, Pignatelli B, Pollock JR, et al. Does increased endogenous formation of N-nitroso compounds in the human colon explain the association between red meat and colon cancer? [J].Carcinogenesis, 1996, 17(3): 515-523.
[35]	Yang T, Owen JL, Lightfoot YL, et al. Microbiota impact on the epigenetic regulation of colorectal cancer [J].Trends Mol Med, 2013, 19(12): 714-725.
[36]	Kumar M, Nagpal R, Verma V, et al. Probiotic metabolites as epigenetic targets in the prevention of colon cancer [J].Nutr Rev, 2013, 71(1): 23-34.
[37]	Ohgaki H, Kusama K, Matsukura N, et al. Carcinogenicity in mice of a mutagenic compound, 2-amino-3-methylimidazo[4,5-f]quinoline, from broiled sardine, cooked beef and beef extract [J].Carcinogenesis, 1984, 5(7): 921-924.
[38]	Hamer HM, Jonkers D, Venema K, et al. Review article: the role of butyrate on colonic function [J]. Aliment Pharmacol Ther, 2008, 27(2):104-119.
[39]	Fung KY, Cosgrove L, Lockett T, et al. A review of the potential mechanisms for the lowering of colorectal oncogenesis by butyrate [J]. Br J Nut, 2012, 108(5): 820-831.
[40]	Beaumont M, Portune KJ, Steuer N, et al. Quantity and source of dietary protein influence metabolite production by gut microbiota and rectal mucosa gene expression: a randomized, parallel, double-blind trial in overweight humans [J].Am J Clin Nutr, 2017, 106(4): 1005-1019.
[41]	Narisawa T, Magadia NE, Weisburger JH, et al. Promoting effect of bile acids on colon carcinogenesis after intrarectal instillation of N-methyl-N'-nitro-N-nitrosoguanidine in rats [J]. J Natl Cancer Inst, 1974, 53(4): 1093-1097.
[42]	Liu L, Zhuang W, Wang RQ, et al. Is dietary fat associated with the risk of colorectal cancer? A meta-analysis of 13 prospective cohort studies [J]. Eur J Nutr, 2011, 50(3): 173-184. URL
[43]	Senok AC, Ismaeel AY, Botta GA. Probiotics: facts and myths [J]. Clin Microbiol Infect, 2005, 11(12): 958-966.
[44]	Kahouli I, Tomaro-Duchesneau C, Prakash S. Probiotics in colorectal cancer (CRC) with emphasis on mechanisms of action and current perspectives [J]. J Med Microbiol, 2013, 62(Pt 8): 1107-1123.
[45]	Hsieh CY, Osaka T, Moriyama E, et al. Strengthening of the intestinal epithelial tight junction by Bifidobacterium bifidum [J]. Physiol Rep, 2015, 3(3): e12327.
[46]	Blackwood BP, Yuan CY, Wood DR, et al. Probiotic lactobacillus species strengthen intestinal barrier function and tight junction integrity in experimental necrotizing enterocolitis [J]. J Probiotics Health, 2017, 5(1): 159.
[47]	Mojka K. Probiotics, prebiotics and synbiotics—Characteristics and functions [J]. Probl Hig Epidemiol, 2014, 95: 541-549.

Please choose a citation manager

Content to export