Colorectal cancer stands as one of the leading malignancies in the digestive system. Over the past decades, Salmonella typhi (S. typhi) and Fusobacterium nucleatum (F. nucleatum) have been discovered to pose risks for colorectal cancer by activating the Wnt/β-catenin pathway. Nevertheless, this revelation represents only a fraction of the influence that the 10¹³ bacteria residing in the intestine exert on the host.

In previous studies, the research team, collaborating with Prof. CHU Bo's group from Shandong University, revealed that the intestinal tract of patients with colorectal cancer was enriched with Peptostreptococcus anaerobius (P. anaerobius). P. anaerobius had a negative impact on tumor prognosis. In fact, not only were there a large number of epithelial cells distributed in the intestine, but more than half of the immune cells and over 70% of T cells in the human body were distributed in the intestine, the largest mucosal immune organ. 

CD8⁺ T cells are crucial immune cells that possess the ability to activate and eliminate tumor cells. In colorectal cancer, the infiltration level and gene expression pattern of CD8⁺ T cells play pivotal roles in determining the prognosis. However, the understanding of the intricate relationship between dysfunctional CD8⁺ T cells within the tumor microenvironment of colorectal cancer and intestinal bacteria/metabolites is limited. And there is a dearth of knowledge regarding the specific bacteria/metabolites that exert an influence on the anti-tumor function of CD8⁺ T cells. 

To identify bacteria and metabolites that regulated the anti-tumor function of CD8⁺ T cells, researchers constructed a library of small-molecule metabolites derived from intestinal microbes. Through rigorous in vitro screening and in vivo validation, they discovered that the secondary bile acid, deoxycholic acid (DCA), produced by C. scindens via the bai operon, effectively suppressed the effector function of CD8⁺ T cells and promoted the growth of colorectal cancer.