吉林大学学报(医学版)

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内质网应激反应蛋白在氧化应激诱导人宫颈癌Hela细胞自噬中的作用

于春艳1，刘希2，于春荣3，张钰4，苏静4，刘玉和1，康劲松4   

  1. （1.北华大学基础医学院病理学教研室，吉林 吉林132013；2. 北华大学化学与生物学院，吉林 吉林132013；3.北京昭衍新药研究中心有限公司毒理部， 北京 100176；4.吉林大学基础医学院病理生理学教研室，吉林 长春 130021）
  • 收稿日期:2013-02-22 出版日期:2014-01-28 发布日期:2014-01-28
  • 通讯作者: 康劲松 E-mail:（Tel:0431-85619485，E-mail:kangjs@jlu.edu.cn)
  • 作者简介:于春艳(1975-),女,吉林省吉林市人，副教授，医学博士，主要从事肿瘤病理学方面的研究。
  • 基金资助:

    国家自然科学基金资助课题（81202552，81272876）；吉林省教育厅基金资助课题（吉教科合字2011第117号，吉教科合字2012第394号）；吉林省科技厅自然科学基金资助课题（201215103，201015200）

Effect of endoplasmic reticulum stress protein in oxidative stress-induced autophagy in human cervical carcinoma Hela cells

YU Chun-yan1,LIU Xi2,YU Chun-rong3,ZHANG Yu4,SU Jing4, LIU Yu-he1,KANG Jin-song4
   

  1. (1. Department of Pathology,School of Basic Medical Sciences,Beihua University,Jilin 132013,China;2. College of Chemistry and Biology,Beihua University,Jilin 132013,China;3.Departmentof Toxicology，Beijing JOINN Laboratories，Beijing 100176,China；4. Department of Pathophysiology,School of Basic Medical Sciences,Jilin University,Changchun 130021,China)
  • Received:2013-02-22 Online:2014-01-28 Published:2014-01-28

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摘要：

目的：探讨内质网应激反应蛋白在氧化应激诱导人宫颈癌Hela细胞自噬过程中的作用，阐明内质网应激-自噬途径调控肿瘤细胞生存的可能机制。方法：人宫颈癌Hela细胞分为对照组、VK3 (30   μmol•L-1)组、内质网应激抑制剂牛磺熊去氧酸钠（TUDC ）(500  μmol•L-1)组和VK3 (30   μmol•L-1)与TUDC(500  μmol•L-1)联合作用组。透射电镜观察Hela细胞内质网形态学变化。MTT 法检测细胞生存率。Western blotting法检测内质网应激特征性分子葡萄糖调节蛋白78（GRP78）和自噬相关蛋白（LC3-Ⅱ）的表达水平。结果：对照组细胞形态正常，VK3组细胞浆内可见自噬泡及扩张的内质网。与VK3组比较，VK3与TUDC联合作用组Hela细胞生存率降低（P<0.05）。与对照组比较，VK3组GRP78和LC3-Ⅱ蛋白表达水平均增加（P<0.05）；与VK3组比较，VK3与TUDC联合作用组 GRP78和LC3-Ⅱ蛋白表达水平均降低（P<0.05）。结论：在氧化应激诱导Hela细胞损伤过程中，内质网应激反应蛋白可介导Hela细胞发生自噬。

关键词: 氧化应激, 内质网, 葡萄糖调节蛋白78, 细胞自噬, Hela细胞

Abstract:

To  investigate the role of endoplasmic reticulum stress protein in oxidative stress-induced autophgy in human cervical carcinoma Hela cells,and to clarify the possible mechanism of endoplasmic reticulum stress-autophagy pathway in regulating the survival of tumor cells.Methods Hela cells were divided into control group,VK3 (30   μmol•L-1) group，ER stress inhibitor TUDC (500  μmol•L-1) group，VK3(30   μmol•L-1) +TUDC(500  μmol•L-1)  group.The morphological changes of endoplasmic reticulum of Hela cells  were observed by transmission electron microscope.The survival rate of Hela cells in each group was measured by MTT assay.The expression levels of glucose-regulated protein-78 (GRP78) and LC3-Ⅱ were determined by Western blotting method.Results The morphology of Hela cells in control group was normal.The autophagic vacuoles and dilated endoplasmic reticulum were observed in cytoplasm of Hela cells in VK3 group.Compared with VK3 group，the survival rate of Hela cells in VK3+ TUDC group was decreased(P<0.05).Compared with control group,the expression levels of GRP78 and LC3-Ⅱ in VK3 group were decreased(P<0.05).Compared with VK3 group,the expression levels of GRP78 and LC3-Ⅱ in TUDC+ VK3 group were decreased (P<0.05).Conclusion Endoplasmic reticulum stress protein can mediate the  autophgy of Hela cells in oxidative stress-induced injury of Hela cells.

Key words: oxidative stress, endoplasmic reticulum, glucose-regulated protein　78, autophagy, Hela cells

中图分类号: 

  • R363.2
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