PIG11与热休克蛋白60的相互作用介导肝癌HepG2细胞凋亡

Interaction of PIG11 and Hsp60 is Involved in Apoptosis in Human Hepatoma HepG2 Cells

为了探讨候选肝癌抑癌蛋白PIG11(p53-induced gene11,PIG11)诱导细胞凋亡的机制,首次在HepG2细胞株中鉴定了11个PIG11结合蛋白,热休克蛋白60(heat shock protein60,Hsp60)为其中之一.采用免疫共沉淀联合Western blot技术对Hsp60进行了验证.用Western blot检测其蛋白质表达,结果显示:pLXSN-PIG11-HepG2细胞中Hsp60蛋白表达较pLXSN-HepG2、HepG2细胞组下调(n=3,P<0.01).选取与Hsp60关系密切的Bax蛋白进行研究,Western blot结果显示PIG11高表达可引起胞浆Bax向线粒体转位.以上结果表明,PIG11蛋白能与HepG2细胞中的Hsp60结合,促进Hsp60-Bax的分离,引起Bax从胞液到线粒体转位,激活线粒体凋亡途径,这可能是其诱导HepG2细胞凋亡的主要机制之一.

In order to explore the mechanisms of candidate liver tumor suppressor protein PIG11 induced apoptosis, eleven PIG11 binding proteins were first time identified in human hepatoma HepG2 cells, which heat shock protein 60 （Hsp60） is one of them. It has been confirmed by co-immunoprecipitation combined with Western blot analysis. Furthermore, using Western blot analysis, the protein expression of lisp60 is down-regulated in pLXSN-PIGll-HepG2 cells group than that of pLXSN-HepG2 and HepG2 groups （n =3, P 〈 0.01）, and over-expression of PIG11 induces translocation of Bax protein from cytoplasm to mitochondria in HepG2 cells. These results suggested that PIG11 protein can combine with Hsp60 in HepG2 cells, and the over-expression of PIG11 induce HepG2 cells apoptosis through mitochondrial pathway and the translocation of Bcl-2 family proteins Bax from cytoplasm to mitochondria maybe play an important role in the process.