p38δ在宫颈癌细胞中的表达及其对缺氧HeLa细胞凋亡的影响

Role of p38δ on hypoxia -induced apoptosis in cervical cancer cells and its effect on hypoxia-mediated apoptosis of HeLa

摘要:

目的探讨p38δ在宫颈癌组织细胞和HeLa细胞系中蛋白表达水平及p38δ对缺氧诱导HeLa细胞凋亡的影响。方法采用蛋白印迹法检测组织及细胞蛋白表达水平。采用慢病毒转染及细胞耐药性筛选构建稳定表达p38δ HeLa细胞株。采用膜联蛋白V-异硫氰酸荧光素/碘化丙啶双染色法检测细胞凋亡水平。结果宫颈癌细胞系HeLa 细胞中p38δ蛋白表达水平低于非癌性细胞系人胚肾293 细胞及小鼠胚胎纤维细胞，差异有统计学意义（P <0.05）；宫颈癌组织细胞中p38δ蛋白表达水平低于正常宫颈组织细胞，差异有统计学意义（P <0.05）；p38δ 过表达提高缺氧条件下HeLa细胞凋亡水平，差异有统计学意义（P <0.05）；p38δ 过表达促进缺氧条件下HeLa 细胞中凋亡相关因子Bcl-2 蛋白表达水平下调及Bax、p53 蛋白表达水平上调，差异有统计学意义（P <0.05）。结论在宫颈癌组织细胞和宫颈癌HeLa 细胞中，p38δ的蛋白表达水平降低。HeLa细胞中高表达p38δ 促进缺氧细胞凋亡。

Abstract:

Objective To investigate the expression level of p38δ cervical cancer cells and its effect on hypoxia-mediated apoptosis of HeLa cells. Methods The expression level of p38δ was identified by Western blot. HeLa cell models stably expressing p38δ were established with lentivirus system. Hypoxia -induced apoptosis in HeLa cells was measured by Annexin V-FITC/PI double labeling system. Results p38δ was significantly down-regulated in cervical cancer tissures and HeLa cells compared with that in normal cervical tissues and non-tumor cell lines, respectively (P < 0.05). Expression of p38δ in cervical cancer tissues was significanthy lower than that in normal cervical tissues. HeLa cells stably expressing p38δ experienced a higher hypoxia-induced apoptosis when compared with control HeLa cells (P < 0.05). Under hypoxia conditions,the expression levels of p53 and Bax in HeLa cells stably expressing p38δ were significantly increased, and Bcl-2 was decreased when compared with those in control HeLa cells (P < 0.05). Conclusions p38δ is downregulated in cervical cancer. Overexpression of p38δ promotes hypoxia-induced apoptosis.