fig1

Roles of gut dysbiosis, anti-proliferative proteins, and post-transcriptional regulation in carcinogenesis

Figure 1. Illustration of the relationship among gut microbiota, cytotoxic T cells, cancer cells, and immune checkpoints inhibitors. There might be two opposite actions of gut microbiota. One is oncogenic or the cancer-causing gut-cancer axis. The other is the gut-anticancer axis favorable to the host. Immune checkpoint molecules are involved in the cell-cell communications, which are present on T cells and shared on cancer cells. Immune checkpoint molecules send signals to inhibit T cell activities of killing cancer cells. Monoclonal antibodies have been used as therapeutic checkpoint inhibitors. Through the gut-anticancer axis, the gut microbiota could activate cytotoxic T cells through undefined mechanisms including the effect of short-chain fatty acids (SCFAs). The arrows indicate stimulation and/or augmentation. Note that some critical events have been omitted for clarity. CTLA4: Cytotoxic T-lymphocyte-associated protein 4; PD1: programmed cell death protein 1; PDL1: programmed cell death ligand 1; CD: cluster of differentiation; ROS: reactive oxygen species.

Journal of Translational Genetics and Genomics
ISSN 2578-5281 (Online)
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