The gut-liver axis: host microbiota interactions shape hepatocarcinogenesis.

Although their etiologies vary, tumors share a common trait: the control of an oncogenic transcriptional program that is regulated by the interaction of the malignant cells with the stromal and immune cells in the tumor microenvironment (TME). The TME shows high phenotypic and functional heterogeneity that may be modulated by interactions with commensal microbes (the microbiota) both systemically and locally. Unlike host cells, the microbiota adapts after environmental perturbations, impacting host-microbe interactions. In the liver, the bidirectional relationship in the gut and its associated microbiota creates an interdependent environment. Therefore, the gut microbiota and its metabolites modulate liver gene expression directly and indirectly, causing an imbalance in the gut-liver axis, which may result in disease, including carcinogenesis.