PAR-4选择性诱导肿瘤细胞凋亡机制的研究进展  

The Progresses on the Prostate Apoptosis Response Protein-4 Inducing Apoptosis Selectively in Cancer Cells and Its Mechanism

作　　者：郭雅馨 孔庆宏[1] 王冠林[1] 

机构地区：[1]昆明理工大学生命科学与技术学院

出　　处：《中国细胞生物学学报》2017年第12期1605-1611,共7页Chinese Journal of Cell Biology

基　　金：国家自然科学基金(批准号:81260351;81360162);云南省科学基金(批准号:2014DA002;2015FB139)资助的课题~~

摘　　要：在肿瘤治疗中,寻找选择性作用于肿瘤细胞的药物是人们所期待和向往的。前列腺凋亡反应蛋白-4(prostate apoptosis response protein-4,Par-4)作为肿瘤抑制因子,能选择性诱导肿瘤细胞凋亡,且在细胞质和细胞核中均可行使其功能。然而有研究发现,Par-4还可以被分泌到细胞外与细胞表面的GRP78相互作用,引起内质网应激,激活FADD/caspase-8/caspase-3通路导致肿瘤细胞凋亡。Par-4在行使其功能的过程中与其他的蛋白质和抗癌药物相互作用,可以协同诱导肿瘤细胞凋亡,为肿瘤治疗提供新的方法和思路。该文就Par-4如何在细胞内外选择性诱导肿瘤细胞凋亡及其与相关基因和其他抗肿瘤药物相互作用的调控机制进行综述。In tumor therapy, looking for a drug that hastheselectively effect on tumor cellsis people expected. As a tumor suppressor the prostate apoptosis response protein-4（Par-4） can selectively induce apoptosis of the tumor cells and play a role in both cytoplasm and nucleus. However, it be found that par-4 can be secreted and interact with the GRP78 onthe cell surface, causing the endoplasmic reticulum stress, which activates the FADD/caspase-8/caspase-3 pathway leading to apoptosis. Par-4 interacts with other proteins and anticancer drugs during the exercise of its function, and they can co-induce tumor cells apoptosis, which provides new methods and ideas for tumor therapy. This paper reviews the regulatory mechanisms of Par-4 on the selective induction of tumor cell apoptosis and its interaction with relevant genes and other antitumor agents.

关 键 词：PAR-4 GRP78 G6PD TRIM21 芳基喹啉 顺铂 

分 类 号：R73-36[医药卫生—肿瘤]