摘要
mTOR接受营养素、生长因子及激素等多种外界信号的刺激,通过激活其下游多种信号分子,在调节细胞的生长、增殖及分化等过程中发挥重要作用。同时,mTOR信号通路亦可调节糖类、脂质及蛋白质三大营养素的代谢过程。既往研究表明,mTOR信号通路中相关基因异常甲基化可促进胃癌、卵巢癌、前列腺癌、乳腺癌及宫颈癌等多种恶性肿瘤的发生及发展,且与患者的临床预后密切相关。为进一步了解mTOR通路中相关基因甲基化与肿瘤之间的联系,本文通过综合分析相关文献后发现,mTOR信号通路中关键节点基因的异常甲基化可导致肿瘤组织发生异常的能量代谢,包括上调肿瘤组织的有氧糖酵解水平,增加肿瘤组织的能量消耗;亦可干扰机体对异常蛋白质水解,从而促进肿瘤组织的生长增殖。因此,可通过抑制mTOR信号通路中相关基因甲基化,进一步逆转肿瘤组织的异常能量代谢状态,从而更有利于治疗肿瘤,改善患者的临床预后。
Stimulated by nutrients, growth factors, hormone and other signals, then by activating its signaling molecules of thedownstream, mTOR plays a critical role in regulating cell growth, proliferation and differentiation. Besides, mTOR signaling pathwaycan also regulate the metabolism of carbohydrate, lipid and protein. Previous studies showed that, the genes methylation of mTORsignaling pathway result in some malignant neoplasms development, such as gastric cancer, ovarian cancer, prostate cancer, breastcancer, cervical cancer and so on, and it is related to the prognosis of patients. In order to understand the association of genes ofmTOR signaling pathway methylation and tumor, we reviewed and analyzed some literatures, then argued that the methylation of keygenes in mTOR signaling pathway could result in abnormal energy metabolism in cancer: producing aerobic glycolysis, increasingthe energy consumption and interfering with protein hydrolysis so that promote the tumor growth. Thus, demethylating genes inmTOR signaling pathway, which might be an entry point to reverse the abnormal energy metabolism in cancer, could be moreconducive to the treatment of cancer and improve the clinical prognosis of patients.
作者
李洁茹
马怀幸
李苏宜
LI Jie-ru;MA Huai-xing;LI Su-yi(Wannan Medical College, Wuhu 241000, Anhui, China;Department of Anhui Provincial Affiliated Hospital of Anhui Medical University (The Western Area) , Hefei 230031, China)
出处
《肿瘤代谢与营养电子杂志》
2016年第3期186-190,共5页
Electronic Journal of Metabolism and Nutrition of Cancer
基金
安徽省自然科学基金项目(1508085MH176)
关键词
MTOR信号通路
甲基化
肿瘤
代谢
mTOR signaling pathway
Methylation
Tumour
Metabolism
作者简介
通讯作者：李苏宜，电子邮箱：njlisuyi@sina.com
