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.

肝细胞癌（HCC）是原发性肝癌的主要形式，也是全球最普遍和威胁生命的恶性肿瘤之一。HCC的标志之一是持续的细胞存活和增殖信号，这取决于致癌基因和肿瘤抑制因子之间的平衡。通过诱导细胞周期停滞，凋亡，细胞衰老或自噬，转化生长因子β（TGF-β）是包括肝细胞在内的上皮细胞的有效生长抑制剂。在肝肿瘤发生过程中，通过多种机制绕过了TGF-β的抗肿瘤作用。此外，随着恶性进展，TGF-β转换以促进癌细胞存活和增殖。TGF-β的这种二分性是肝癌治疗靶向的障碍之一。之后，了解潜在的分子机制是发现新的抗肿瘤药物的先决条件，这些药物可能会特异性地破坏TGF-β信号的生长促进分支或恢复其肿瘤抑制臂。这篇综述总结了TGF-β如何抑制或促进肝癌细胞的存活和增殖，突出了该过程中的功能转换机制。