过氧化物酶V在顺铂诱导HepG2肝癌细胞凋亡过程中的调控作用

The Role of Peroxiredoxin V in Cisplain-Induced Human Liver Cancer Cell Line HepG2 Apoptosis

过氧化物酶V(peroxiredoxin V, Prx V)是过氧化物酶家族(peroxiredoxins, Prxs)中的一员,具有清除细胞内活性氧(reactive oxygen species, ROS)的功能。该文主要阐明了Prx V在顺铂(cisplatin, CDDP)诱导Hep G2人肝癌细胞凋亡过程中的调控作用。该研究利用顺铂处理Hep G2肝癌细胞,通过荧光显微照相、流式细胞术、蛋白质免疫印迹分析等方法检测细胞内活性氧(ROS)水平、细胞凋亡情况以及凋亡相关蛋白水平。研究结果表明,顺铂可引起细胞内的ROS水平升高导致细胞凋亡,同时造成细胞内Prx V蛋白质表达水平下降。利用慢病毒载体过量表达Prx V基因后,顺铂诱导的Prx V过量表达型HepG2细胞凋亡率明显低于Mock组,同时促凋亡蛋白cleavage-Caspase-3、Bad、cleavage-PARP表达水平也明显被下调,说明Prx V在顺铂诱导HepG2细胞凋亡过程中具有一定的抑制作用。该研究初步探究了Prx V在顺铂诱导的HepG2肝癌细胞凋亡过程中的调控作用,为肝癌的治疗研究提供了新的思路和治疗靶点。

Peroxiredoxin V(Prx V) is a member of the Peroxiredoxin families(Prxs) and plays a role on scavenging the intracellular reactive oxygen species(ROS).In the current study,we observed the regulatory role of Prx V on the apoptosis of HepG2 human liver cancer cells induced by cisplatin(CDDP).The CDDP induced cellular ROS,apoptosis and apoptosis related proteins expression levels were measured by fluorescence microscopy,flow cytometry and Western blot analysis.The results indicated that cisplatin could induce the HepG2 cell apoptosis by accumulating the intracellular ROS levels,while the protein expression level of Prx V was down-regulated.After over-expressed of the Prx V gene with lentivirus,the CDDP induced HepG2 cell apoptosis was decreased in Prx V over-expressed cells compared with that of mock cells.The pro-apototic proteins,such as cleavage-Caspase-3,Bad and cleavage-PARP expression levels were also significantly down-regulated in Prx V(O/V) cells than Mock cells.Our findings demonstrated the protective role of Prx V on CDDP induced HepG2 cell apoptosis and gave a new sight to treatment of the liver cancers.