Propofol inhibits tumor angiogenesis through targeting VEGF/VEGFR and mTOR/eIF4E signaling.

Propofol, a commonly used intravenous anesthetic in tumor surgery, has recently garnered attention for its anti-cancer activity. We previously demonstrated that propofol inhibits migration and invasion of esophageal squamous cell carcinoma cells. However, the effects of propofol in tumor angiogenesis are inconclusive. The current study investigated the effects of propofol on the biological functions of lung cancer associated endothelial cells (LC-EC) and colon cancer associated endothelial cells (CC-EC) that represent in vitro tumor angiogenesis. We showed that propofol inhibited tubular structure formation of both LC-EC and CC-EC, particularly the early stages of angiogenesis. In addition, propofol inhibited migration, adhesion, proliferation, and survival of tumor associated endothelial cells. Mechanism studies revealed that propofol disrupted tumor angiogenesis microenvironment via suppressing expression and secretion of multiple pro-angiogenic factors by tumor cells. Propofol also inhibited VEGF/VEGFR2-and mTOR/eIF4E-mediated signaling pathways in endothelial cells. Our findings demonstrate the inhibitory effects of propofol on tumor angiogenesis and support the anti-cancer properties of propofol. Our work provides preclinical evidence into the potential mechanisms by which propofol may negatively affect tumor growth and metastasis. • Propofol inhibits tumor angiogenesis. • Propofol inhibits tumor endothelial cell migration, adhesion and growth. • Propofol disrupts tumor angiogenesis microenvironment. • Propofol inhibits VEGF/VEGFR- and mTOR/eIF4E-mediated signaling. [ABSTRACT FROM AUTHOR]