肿瘤细胞和正常细胞相比的一个重要特点就是肿瘤细胞的代谢异常。而其中肿瘤细胞的脂代谢异常在肿瘤的发生发展过程中发挥着重要的作用。然而，人们对肿瘤细胞的脂代谢异常的认识还不清晰。近期有研究提示，组蛋白甲基转移酶G9a参与正常细胞的脂肪代谢过程，但具体机制尚不清楚，尤其是G9a在肿瘤脂代谢中的作用及生物学意义有待进一步探索。我们的前期研究结果表明：（1）在细胞代谢物油酸(OA)和软脂酸(PA)处理的情况下，G9a在染色质上的富集升高，相应H3K9me2也明显升高；（2）G9a能够与蛋白激酶CK2相互结合，并被CK2磷酸化，磷酸化位点是Ser211；（3）G9a的Ser211磷酸化与G9a的染色质定位密切相关。课题将以前期工作为基础，深入探讨G9a参与肿瘤脂代谢的分子机制，寻找G9a参与调节的脂代谢相关基因，为临床肿瘤治疗提供新途径，并为将来以G9a为靶点的药物研发提供新思路。

Abnormal metabolism is one of the most important characteristics of tumor cells, compared to that of normal cells. And Lipid metabolic abnormalities play a critical role in the process of tumor development. However, it is largely unknown that how lipid metabolism affected cancer development. Recent studies suggest that histone methyltransferase G9a is involved in lipid metabolism in normal cells, but the molecular mechanism is not clear, and the role of G9a in tumor lipid metabolism has not been illustrated yet. Our preliminary results indicate that: (1) The enrichment of G9a on the chromatin increased in response to oleic acid (OA) or palmitic acid (PA) treatment, and correspondingly, the level of H3K9me2 was induced as well. (2) G9a was interacted with protein kinase CK2, and phosphorylated by CK2 at Ser211. (3) Ser211 phosphorylation is closely related to the chromatin localization of G9a. Based on our preliminary work, we will further explore the molecular mechanism by which G9a is involved in cancer lipid metabolism. This work will provide a new clue for clinical cancer therapy and new strategy for drug development targeting G9a.