Dysbiosis of the gut microbiome has been associated with the development of colorectal cancer (CRC). Gut microbiota is involved in the metabolic transformations of dietary components into oncometabolites and tumor-suppressive metabolites that in turn affect CRC development. In a healthy colon, the major of microbial metabolism is saccharolytic fermentation pathways. The alpha-bug hypothesis suggested that oncogenic bacteria such as enterotoxigenic Bacteroides fragilis (ETBF) induce the development of CRC through direct interactions with colonic epithelial cells and alterations of microbiota composition at the colorectal site. Escherichia coli, E. faecalis, F. nucleatum, and Streptococcus gallolyticus showed higher abundance whereas Bifidobacterium, Clostridium, Faecalibacterium, and Roseburia showed reduced abundance in CRC patients. The alterations of gut microbiota may be used as potential therapeutic approaches to prevent or treat CRC. Probiotics such as Lactobacillus and Bifidobacterium inhibit the growth of CRC through inhibiting inflammation and angiogenesis and enhancing the function of the intestinal barrier through the secretion of short-chain fatty acids (SCFAs). Crosstalk between lifestyle, host genetics, and gut microbiota is well documented in the prevention and treatment of CRC. Future studies are required to understand the interaction between gut microbiota and host to the influence and prevention of CRC. However, a better understanding of bacterial dysbiosis in the heterogeneity of CRC tumors should also be considered. Metatranscriptomic and metaproteomic studies are considered a powerful omic tool to understand the anti-cancer properties of certain bacterial strains. The clinical benefits of probiotics in the CRC context remain to be determined. Metagenomic approaches along with metabolomics and immunology will open a new avenue for the treatment of CRC shortly. Dietary interventions may be suitable to modulate the growth of beneficial microbiota in the gut.

肠道微生物群的失调与结直肠癌 (CRC) 的发展有关。肠道微生物群参与将膳食成分代谢转化为癌代谢物和肿瘤抑制代谢物，进而影响 CRC 的发展。在健康的结肠中，微生物代谢的主要途径是糖分解发酵途径。α-bug 假说表明，致癌细菌，如产肠毒素脆弱类杆菌(ETBF)，通过与结肠上皮细胞的直接相互作用和结肠直肠部位微生物群组成的改变，诱导 CRC 的发展。大肠杆菌，ē。粪肠球菌，F。成核，和在 CRC 患者中，链球菌 gallolyticus显示出更高的丰度，而双歧杆菌、梭状芽孢杆菌、粪杆菌和Roseburia显示出丰度降低。肠道微生物群的改变可用作预防或治疗 CRC 的潜在治疗方法。益生菌，如乳酸杆菌和双歧杆菌通过抑制炎症和血管生成以及通过分泌短链脂肪酸 (SCFA) 增强肠道屏障的功能来抑制 CRC 的生长。生活方式、宿主遗传学和肠道微生物群之间的串扰在 CRC 的预防和治疗中得到了充分证明。未来的研究需要了解肠道微生物群与宿主之间的相互作用对 CRC 的影响和预防。然而，还应考虑更好地了解 CRC 肿瘤异质性中的细菌失调。元转录组学和元蛋白质组学研究被认为是了解某些细菌菌株抗癌特性的强大组学工具。益生菌在 CRC 中的临床益处仍有待确定。宏基因组学方法以及代谢组学和免疫学将很快为 CRC 的治疗开辟一条新途径。饮食干预可能适合调节肠道有益微生物群的生长。