TP53诱导的糖酵解与凋亡调控因子在恶性肿瘤中的研究进展  

Research Progress of TP53-induced Glycolysis and Apoptosis Regulatory Factors in Malignant Tumors

作　　者：冯振兴[1] 田铁栓[1] FENG Zhen-xing;TIAN Tie-shuan(Tianjin Chest Hospital/Tianjin Institute of Cardiovascular Diseases,Tianjin 300222,China)

机构地区：[1]天津市胸科医院/天津市心血管病研究所,天津300222

出　　处：《医学信息》2021年第13期33-37,共5页Journal of Medical Information

摘　　要：TP53诱导的糖酵解与凋亡调控因子(TIGAR)的结构与2,6-磷酸果糖激酶类似,其基本功能是通过抑制糖酵解调节磷酸戊糖途径产生大量的NADPH及合成DNA所需的核糖,从而降低活性氧簇(ROS)诱导的细胞损伤,促进DNA损伤修改和细胞增殖。TIGAR作为ROS限制性蛋白,主要参与肿瘤细胞的凋亡、自噬的调控,并且与MAPK-ERK、PI3K-AKT和NF-κB等多个信号通路有关,在肿瘤的增殖、侵袭及转移中发挥重要作用。此外,TIGAR高表达降低了与肿瘤对顺铂、5-FU、替莫唑胺、PARP(多聚ADP核糖多聚酶)抑制剂、内分泌治疗以及放射治疗的敏感性,与肿瘤患者的病理分期晚、远处转移和生存预后差等密切相关。本文拟对上述问题进行综述,探讨TIGAR作为肿瘤治疗靶点的潜在应用价值。The structure of TP53-induced glycolysis and apoptosis regulator(TIGAR)is similar to that of 2,6-phosphofructokinase.Its basic function is to regulate the pentose phosphate pathway by inhibiting glycolysis,which is required for the production of large amounts of NADPH and the synthesis of DNA.Ribose,thereby reducing cell damage induced by reactive oxygen species(ROS),and promoting DNA damage modification and cell proliferation.TIGAR,as a ROS-restricted protein,is mainly involved in the regulation of tumor cell apoptosis and autophagy,and is related to multiple signaling pathways such as MAPK-ERK,PI3K-AKT and NF-κB,and plays a role in tumor proliferation,invasion and metastasis Important role.In addition,the high expression of TIGAR reduces the sensitivity of tumors to cisplatin,5-FU,temozolomide,PARP(poly ADP ribose polymerase)inhibitors,endocrine therapy and radiation therapy,and is related to the late pathological staging and distant metastasis of tumor patients.It is closely related to poor survival prognosis.This article intends to review the above issues and discuss the potential application value of TIGAR as a tumor treatment target.

关 键 词：TIGAR TP53 恶性肿瘤 凋亡调控因子 

分 类 号：R730.22[医药卫生—肿瘤]