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Guillermou
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Lifestyle, diet, and genetics are established risk factors for the development of colorectal cancer (CRC). In recent years, the role of the gut microbiota (GM) has been increasingly highlighted in various studies, suggesting an impact on both disease pathogenesis and the efficacy and tolerability of treatments. We conducted a Medline search to identify published studies exploring the role of GM in the development and treatment of CRC. Dysbiosis, an imbalance in GM, is common in patients with CRC and is associated with precancerous lesions, aggressive tumors, and diverse therapeutic outcomes. Restoring GM balance can reduce treatment complications and improve prognosis. This review details how GM influences CRC through metabolite production, modulation of inflammation, and alteration of the immune response. Diet significantly influences MF composition: processed meats and high-fat diets increase the risk of CRC, while high-fiber diets have a protective effect. The role of MF in CRC treatments, such as surgery, chemotherapy, radiotherapy, and immunotherapy, is also explored, highlighting its influence on complications, chemoresistance, and treatment efficacy. Future strategies involving MF modulation through diet, probiotics, and fecal microbiota transplantation (FMT) hold promise for CRC prevention and treatment, warranting further investigation.

Studies have suggested that a high-fat diet (HFD) results in gut microbial alterations. HFD-related gut bacterial changes may influence gut secretory, absorptive, and immune functions. HFD may regulate gut microbial composition and intestinal inflammation, increasing gut susceptibility to carcinogenic factors and exacerbating CRC. The fecal microbiota of CRC patients could increase polyp numbers and promote intestinal dysplasia and proliferation, as well as inflammatory markers, in germ-free and conventional mice; this indicates that changes in the gut microbiota can induce intestinal inflammation and carcinogenesis. As a major product of the Gram-negative gut microbiota, lipopolysaccharides (LPS) promote intestinal inflammation and CRC progression. An inflammatory microenvironment shaped by the gut microbiota can promote tumorigenesis in the colorectum. Altered gut microbiota is associated with metabolic diseases and cancers, including breast, liver, and colorectal cancers. Particularly in CRC, there is an abundance of flora, including Bacteroides fragilis, Escherichia coli, Streptococcus gallolyticus, Enterococcus faecalis, and Fusobacterium nucleatum. Short-chain fatty acids (SCFAs) are widely investigated metabolites of the gut microbiota, which can protect the intestinal mucosa from inflammation. As a SCFA, butyrate inhibits CRC tumor progression through multiple mechanisms, including anti-inflammatory and immunomodulatory effects.

This study demonstrated high-fat diet-induced changes in the colorectal and liver microenvironments. Furthermore, we initially demonstrated DSV enrichment in fecal samples from patients with CRC liver metastases and investigated the DSV (Desulfovibrio)-induced pro-metastatic microenvironment in the liver. This study could pave the way for investigating high-fat diet-induced gut microbiota disorders, especially DSV abundance, in CRC liver metastases. It provided a reference for assessing the potential for liver metastasis in CRC. However, research was limited by a lack of exploration of the underlying mechanisms; Further research is needed to determine the mechanisms by which high-fat diets and VSD promote carcinogenesis and metastasis in CRC.

A high-fat diet may induce alterations in the gut microbiota, reflected in an increase in Gram-negative microbiota. Furthermore, a high-fat diet may induce colonic inflammation, barrier dysfunction, and remodeling of the liver microenvironment, by modifying the gut microbiota and promoting CRC initiation and liver metastasis. VSD may also play a crucial role in CRC initiation and promoting a pre-metastatic microenvironment in the liver.

https://www.mdpi.com/2072-6694/14/11/2573 (2022).--

https://www.mdpi.com/2076-2607/13/6/1410 (2025).--

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