Sánchez-Alcoholado Lidia, Ramos-Molina Bruno, Otero Ana, Laborda-Illanes Aurora, Ordóñez Rafael, Medina José Antonio, Gómez-Millán Jaime, Queipo-Ortuño María Isabel
Unidad de Gestión Clínica Intercentros de Oncología Médica, Hospitales Universitarios Regional y Virgen de la Victoria. Instituto de Investigación Biomédica de Málaga (IBIMA)-CIMES-UMA, 29010 Málaga, Spain.
Departamento de Cirugía Digestiva, Endocrina y Transplante de Órganos Abdominales, Instituto Murciano de Investigación Biosanitária (IMIB-Arrixaca), 30120 Murcia, Spain.
Cancers (Basel). 2020 May 29;12(6):1406. doi: 10.3390/cancers12061406.
Colorectal cancer (CRC) is the third most common cancer worldwide and the leading cause of cancer-related deaths. Recently, several studies have demonstrated that gut microbiota can alter CRC susceptibility and progression by modulating mechanisms such as inflammation and DNA damage, and by producing metabolites involved in tumor progression or suppression. Dysbiosis of gut microbiota has been observed in patients with CRC, with a decrease in commensal bacterial species (butyrate-producing bacteria) and an enrichment of detrimental bacterial populations (pro-inflammatory opportunistic pathogens). CRC is characterized by altered production of bacterial metabolites directly involved in cancer metabolism including short-chain fatty acids and polyamines. Emerging evidence suggests that diet has an important impact on the risk of CRC development. The intake of high-fiber diets and the supplementation of diet with polyunsaturated fatty acids, polyphenols and probiotics, which are known to regulate gut microbiota, could be not only a potential mechanism for the reduction of CRC risk in a primary prevention setting, but may also be important to enhance the response to cancer therapy when used as adjuvant to conventional treatment for CRC. Therefore, a personalized modulation of the pattern of gut microbiome by diet may be a promising approach to prevent the development and progression of CRC and to improve the efficacy of antitumoral therapy.
结直肠癌(CRC)是全球第三大常见癌症,也是癌症相关死亡的主要原因。最近,多项研究表明,肠道微生物群可通过调节炎症和DNA损伤等机制,以及产生参与肿瘤进展或抑制的代谢产物,来改变CRC的易感性和进展。在CRC患者中观察到肠道微生物群失调,共生细菌种类(产丁酸细菌)减少,有害细菌群体(促炎机会性病原体)增多。CRC的特征是直接参与癌症代谢的细菌代谢产物(包括短链脂肪酸和多胺)的产生发生改变。新出现的证据表明,饮食对CRC发生风险有重要影响。高纤维饮食的摄入以及用已知可调节肠道微生物群的多不饱和脂肪酸、多酚和益生菌补充饮食,不仅可能是在一级预防中降低CRC风险的潜在机制,而且在用作CRC传统治疗的辅助手段时,对增强癌症治疗反应也可能很重要。因此,通过饮食对肠道微生物组模式进行个性化调节,可能是预防CRC发生和进展以及提高抗肿瘤治疗疗效的一种有前景的方法。