Figure 2.
Gut microbes and metabolites in HCC inhibition. Gut microbes, through the fermentation of dietary fiber, yield SCFAs, which fortify intestinal epithelial barrier function by upregulating tight junction protein expression and mitigating intestinal inflammatory responses. This concerted action reduces the infiltration of carcinogenic agents and diminishes the chronic inflammatory milieu within the liver, thereby exerting a suppressive effect on HCC development. Probiotics, by curtailing histone deacetylase activity, augment histone acetylation, thus facilitating DNA repair and promoting cancer cell apoptosis. Moreover, probiotics modulate the expression of key genes and Kirsten rat sarcoma viral oncogene homolog, further influencing cancer cell growth and impeding proliferation. Metabolites derived from gut microbes, by mediating DNA damage repair, modulating the phosphatidylinositol 3-kinase/protein kinase B signaling axis, and suppressing pro-growth signals, such as MYC proto-oncogene, bHLH transcription factor and NF-κB, consequently restrain HCC cell proliferation. Furthermore, gut microbes, by refining the tumor microenvironment and bolstering anti-tumor immune responses, amplify the anti-tumorigenic effects of effector T cells, thereby impeding both the occurrence and progression of HCC.
