山西医科大学学报2012，Vol.43Issue(11)：808-812,885,6.DOI:10.3969/J.ISSN.1007-6611.2012.11.002
内质网应激-自噬反应在顺铂诱导宫颈癌HeLa细胞死亡中的作用
Role of endoplasmic reticulum stress-autophagic response in cisplatin-induced cervical cancer HeLa cells death
摘要
Abstract
Objective To investigate the role of endoplasmic reticulum(ER) stress - autophagic response in cisplatin-induced cervical cancer HeLa cell death, and to explore the effect of Beclin 1 on sensitivity of HeLa cells to cisplatin. Methods Hela cells were treat ed with different concentrations of cisplatin, respectively. Monodansylcadaverin (MDC) method was explored to measure the formation of autophagic vacuoles, and Western blot was used to detect the protein expression of Beclin 1, LC3 ,IRE1, PERK and ATF6. The eu-karyotic expression vector of Beclin 1 was transfected via lipofectamine into HeLa cells, MTT assay was employed to observe the effect of cisplatin on the IC50 of HeLa cells, and flow cytometry was used to observe the percentage of autophagic cells and apoptotic cells. Results The autophagosomes were increased after treated with cisplatin, and the expression of Beclin 1 and LC3 was significantly increased in a dose-dependent manner in HeLa cells (P ＜0. 05) , while the expression of IRE 1, PERK and ATF6 was increased too. The the expression of Beclinl significantly increased after pcDNA3. 1 ( + )-Beclinl vector being transfected into HeLa cells (P ＜ 0.05). MTT assay showed the IC50 value decreased from 1.0 μg/ml to 0. 5 μg/ml, and more apoptotic cells were identified after pcD-NA3. 1 ( + ) - Beclinl being transfected (P ＜0. 05). Conclusion ER stress-autophagic response plays an important role in the process of cisplatin-induced HeLa cells death, and Beclin 1 overexpression can increase the sensitivity of HeLa cells to cisplatin.关键词
Beclin 1/顺铂/内质网应激/自噬/宫颈癌Key words
Beclin 1/ cisplatin/ ER stress/ autophagy/ cervical cancer分类
医药卫生引用本文复制引用
王赞宏,张晶,白淘..内质网应激-自噬反应在顺铂诱导宫颈癌HeLa细胞死亡中的作用[J].山西医科大学学报,2012,43(11):808-812,885,6.基金项目
山西省科技攻关基金资助项目(20120313019-2) （20120313019-2）
山西省卫生厅攻关基金资助项目(2011024) （2011024）
