糖脂代谢异常是肿瘤的一个重要特征。低氧诱导因子1（HIF1）在肿瘤糖脂代谢异常中起关键调节作用。最近研究发现低氧下HIF1通过调控逆转式三羧酸循环促进细胞内新生脂肪酸的合成，但尚无HIF1直接调控脂肪酸合成的报道。我们的前期研究发现低氧诱导的脂积累依赖于HIF1的活性，并且低氧下HIF1可以调控脂肪酸合成相关基因硬脂酰辅酶A去饱和酶1（SCD1）的表达。本研究将利用细胞系深入研究HIF1调控SCD1表达的机制以及SCD1在低氧诱导脂积累中的作用，探讨SCD1对血管生成的影响；并进一步用原发性肝细胞肝癌样本和二乙基亚硝胺诱导的小鼠肝癌模型研究HIF1和SCD1在肿瘤脂积累以及血管生成中的作用，探索SCD1作为肝癌防治靶点的可行性。本研究不仅对揭示HIF1和SCD1在低氧诱导脂积累中的作用以及SCD1与血管生成的关系具有重要理论意义，而且可能为肿瘤的防治提供新的策略与思路。

Metabolism disorders of glucose and lipids are one of the important features of tumors. Hypoxia-induced factor 1 (HIF1) plays a central role in metabolism disorders of glucose and lipids of tumors. Recently some researchers found that HIF1 regulates de novo fatty acid synthesis through regulating tricarboxylic acid (TCA) cycle reverse under hypoxia; however, there is no report about HIF1 regulating fatty acid synthesis-related genes directly. Here, we found that hypoxia-induced lipid accumulation depends on HIF1's activity, and HIF1 could regulate the expression of stearoyl-CoA desaturases (SCD1), a fatty acid synthesis-related gene, under hypoxia. Based on these findings, we will study the mechanism by which HIF1 regulates SCD1 and the role of SCD1 in hypoxia-induced lipid accumulation; and we will explore the role of SCD1 in angiogenesis in cell lines. Furthermore, we will employ primary hepatocellular carcinoma samples and a mouse hepatocarcinoma model induced by diethylnitrosamine to study the roles of HIF1 and SCD1 in lipid accumulation and angiogenesis of tumors, and also to explore the possibllity of SCD1 as a target for prevention and treatment in liver cancer.This study will not only be of important theoretical significance in revealing the roles of HIF1 and SCD1 in hypoxia-induced lipid accumulation and the relationship between SCD1 and angiogenesis, but will also provide new strategies and ideas for the prevention and treatment of tumors.