Activated platelets contribute to the progression of hepatocellular carcinoma by altering the tumor environment

Abstract Aim Hepatocellular carcinoma (HCC) is a primary liver cancer that usually develops in background of chronic disease and prolonged inflammation. A major contributor the complex molecular pathogenesis HCC highly intertwined cross-talk between tumor surrounding stromal cells, such as hepatic stellate endothelial macrophages other immune cells. These tumor-stroma interactions actively fuel growth modulate microenvironment to benefit invasion progression. Platelets have been reported interact with different cell types microenvironment, including cells macrophages. Materials methods Mice were treated hepatocarcinogenic compound diethylnitrosamine for 25 weeks induce fibrosis From week 10, anti-platelet drug Clopidogrel was added drinking water mice given ad libitum access. Key findings In this study, we show activated platelets promote proliferation contribute adverse fuels We also inhibiting platelet activation P2Y12-inhibitor decreases number tumors chemically induced mouse model HCC. Significance results suggest an important role use drugs may be therapeutically relevant patients cancer.