肿瘤甲硫氨酸依赖性分子机制的研究进展

Molecular mechanisms of cancer cell methionine dependence

甲硫氨酸(M et)依赖性是肿瘤代谢缺陷的重要特征之一。近年来,从分子水平对肿瘤细胞的M et依赖性进行一系列研究,发现了M et代谢的关键酶功能异常(如M et合成酶单核苷酸多态性,甲基硫腺苷磷酸酶基因缺失,胸苷合成酶蛋白表达下降,甲叉四氢叶酸还原酶基因表达上调)。细胞内信号转导障碍是M et限制导致肿瘤细胞凋亡的另一分子机制。

Methionine dependence is one of characteristic metabolism deficiency in cancer cells. Recently a series of researches focusing on key enzymes of methionine metabolism demonstrated that several molecular events might relate with cancer cell methionine dependence（ i. e. , methionine synthase single nucleotide polymorphism , methythioadenosine phophorylase gene deletion, down regulation of thymidylate synthase translation ; up regulation of methylenetetrahydrofolate reductase expression） . Cell apoptosis induced by intracellular signal transduction dysfunction might be another potential mechanism.