Platelet C3G protects from liver fibrosis, while enhancing tumor growth through regulation of the immune response.

ABSTRACT: Primary liver cancer usually occurs in the context of chronic liver disease (CLD), in association with fibrosis. Platelets have emerged as important regulators of CLD and liver cancer, although their precise function and mechanism of action need to be clarified. C3G (RapGEF1) regulates platelet activation, adhesion, and secretion. Here we evaluate the role of platelet C3G in chemically induced fibrosis and liver cancer associated with fibrosis using genetically modified mouse models. We found that while overexpression of full-length C3G in platelets decreased liver fibrosis induced by chronic treatment with CCl₄, overexpressed C3G lacking the catalytic domain did not, although in both cases platelet recruitment to the liver was similar. In addition, C3G deletion in platelets (PF

SUBMITTER: Baquero C 

PROVIDER: S-EPMC11880977 | biostudies-literature | 2025 Apr

REPOSITORIES: biostudies-literature