Hepatocellular carcinoma (HCC) is the major form of primary liver cancer and one of the most prevalent and life-threatening malignancies globally.One of the hallmarks in HCC is the sustained cell survival and proliferative signals,which are determined by the balance between oncogenes and tumor suppressors.Transforming growth factor beta (TGF-β) is an effective growth inhibitor of epithelial cells including hepatocytes,through induction of cell cycle arrest,apoptosis,cellular senescence,or autophagy.The antitumorigenic effects of TGF-β are bypassed during liver tumorigenesis via multiple mechanisms.Furthermore,along with malignant progression,TGF-β switches to promote cancer cell survival and proliferation.This dichotomous nature of TGF-β is one of the barriers to therapeutic targeting in liver cancer.Thereafter,understanding the underlying molecular mechanisms is a prerequisite for discovering novel antitumor drugs that may specifically disable the growth-promoting branch of TGF-β signaling or restore its tumor-suppressive arm.This review summarizes how TGF-β inhibits or promotes liver cancer cell survival and proliferation,highlighting the functional switch mechanisms during the process.