Liu Qian, Dong Xifeng
Tianjin Lung Cancer Institute, Tianjin Medical University General Hospital, Tianjin 300020, People's Republic of China.
Department of Hematology, Tianjin Medical University General Hospital, Tianjin 300020, People's Republic of China.
J Hepatocell Carcinoma. 2021 Jan 28;8:19-21. doi: 10.2147/JHC.S278517. eCollection 2021.
Hepatocellular carcinoma (HCC) is one of the most common and serious types of cancer in the world. Currently, the treatment options for patients with HCC are limited. Lipid metabolic alterations are being recognized as a therapeutic target in the past few years. De novo lipogenesis has been frequently observed in HCC. Fatty acid synthase (FASN) is the key enzyme of de novo lipogenesis. Previous studies have indicated that loss of FASN suppresses the growth of HCC cells, but it cannot completely prevent HCC formation in vivo. Thus, other mechanisms that can support HCC tumor formation in the absence of de novo lipogenesis maybe existed. In a study recently published in Gut, Che and colleague investigated the functions of Fasn in HCC mouse model and explore the crosstalk between de novo lipogenesis and cholesterol biosynthesis-associated pathway during HCC development. These findings highlight the simultaneous inhibition of de novo lipogenesis and cholesterol biosynthesis as a novel therapeutic and prevention strategy for HCC.
肝细胞癌（HCC）是世界上最常见且最严重的癌症类型之一。目前，HCC患者的治疗选择有限。在过去几年中，脂质代谢改变正被视为一种治疗靶点。在HCC中经常观察到从头脂肪生成。脂肪酸合酶（FASN）是从头脂肪生成的关键酶。先前的研究表明，FASN的缺失会抑制HCC细胞的生长，但它不能完全阻止体内HCC的形成。因此，可能存在其他在缺乏从头脂肪生成的情况下支持HCC肿瘤形成的机制。在最近发表于《肠道》杂志的一项研究中，Che及其同事研究了Fasn在HCC小鼠模型中的功能，并探索了HCC发生过程中从头脂肪生成与胆固醇生物合成相关途径之间的相互作用。这些发现突出了同时抑制从头脂肪生成和胆固醇生物合成作为一种针对HCC的新型治疗和预防策略。
