A new aspect of the human body disengages an ecosystem, established by a symbiotic relationship between the host and the gut microbiota. This interaction accounts for maintaining homeostasis in the host and provides a nutrient-rich setting for the microbiota. The gut microbiome’s aberrant microbial composition and metabolic activity have been implicated as risk factors or the consequences of several diseases in humans, such as inflammatory bowel disease (IBD) and colorectal cancer. Therefore, precision modification of the gut microbiota is a potential approach for maintaining human health and disease prevention and treatment. There has been a growing interest in identifying the impact of vitamin D deficiency on carcinogenesis in cancer research. Vitamin D exerts its biological functions by binding to the nuclear receptor, vitamin D receptor (VDR).
The results confirm that dysbiosis in mice with VDR deletion in intestinal epithelial cells promotes tumorigenesis through stimulating anti-inflammatory JAK/STAT3 signaling. It has been reported that alterations in the metabolism, distribution, or composition of the gut microbiota may produce an environment in the colon that promotes cancer, dysplasia, and inflammation.
In conclusion, patients with IBD are at increased risk of colorectal cancer. The JAK/STAT inhibitors could be combined with VDR activators for preventing the development of colitis-associated colorectal cancer and treating chronic inflammation. Therefore, mechanistic understanding of the symbiotic relationship between the gut microbiota and the host could lay a foundation for investigating the pathogenesis of diseases related to dysbiosis and manipulating the gut microbiota as an approach to disease prevention and treatment.