吉林大学学报(医学版)

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埃克替尼通过p38-MAPK信号通路对涎腺腺样囊性癌ACC-M细胞的凋亡诱导作用

杨彩玲1,张景航2,张应花3,任铭新3,刘进忠4,崔卫刚3   

  1. 1.  新乡医学院第一附属医院口腔外科,河南 新乡 453100;2.新乡医学院病理科,河南 新乡 453003;3.新乡医学院人体解剖学教研室,河南 新乡 453003;4.郑州大学口腔医学院口腔病理教研室,河南 郑州 450052
  • 收稿日期:2014-04-21 出版日期:2014-07-28 发布日期:2015-01-18
  • 通讯作者: 崔卫刚(Tel:0373-3329252,E-mail:cuiweigang1978@126.com) E-mail:cuiweigang1978@126.com
  • 作者简介:杨彩玲(1970-),女,河南省新乡市人,医学硕士,副教授,主要从事口腔肿瘤发病机制的研究。
  • 基金资助:

    河南省教育厅科学技术研究重点项目资助课题(14B320018)

Induction effect of icotinib on apoptosis of salivary adenoid
 cystic carcinoma ACC-M cells through p38-MAPK pathway


YANG Cai-ling1,ZhANG Jing-hang2,ZHANG Ying-hua3,REN Ming-xin3,LIU Jin-zhong4,CUI Wei-gang3   

  1. 1.Department of Oral and Maxillofacial Surgery,First Affiliated Hospital,Xinxiang Medical 
    University,Xinxiang 453100,China;2.Department of Pathology,Xinxiang Medical University,
    Xinxiang 453003,China;3.Department of Human Anatomy,Xinxiang Medical University,Xinxiang 
    453003,China;4.Department of Oral Pathology,College of Stomatology,Zhengzhou University,Zhengzhou 450052,China
  • Received:2014-04-21 Online:2014-07-28 Published:2015-01-18

摘要:

目的:探讨埃克替尼对人涎腺腺样囊性癌细胞ACC-M凋亡的影响,阐明埃克替尼对涎腺腺样囊性癌的治疗作用机制。方法:ACC-M细胞随机分为对照组,2、4、8 μmo1/L-1埃克替尼组,促分裂原活化蛋白激酶(APK)抑制剂SB203580(20 μmol/L-1)组,SB203580(20 μmol/L-1 )+埃克替尼(4 μmol/L-1 )组。4 h后收
集细胞,采用MTT法检测各组ACC-M细胞的生长抑制率,用caspase-3活力检测试剂盒检测ACC-M细胞的凋亡情况( 即caspase-3活力),采用
Western blotting法检测p-p38-MAPK蛋白的表达水平。结果:与对照组比较,埃克替尼组ACC-M细胞生长抑制率明显升高(P<0.05),caspase-3活力显著增强(P<0.05),
p-p38-MAPK蛋白表达水平增加(P<0.05)。与4 μmol/L-1 埃克替尼组比较,SB203580+埃克替尼组p-p38-MAPK蛋白表达水平明显降低(P<0.05),caspase-3活力显著降低(P<0.05)。结论:埃克替尼可通过上调p-p38-MAPK信号的表达诱导ACC-M细胞凋亡。

关键词:  , 埃克替尼;涎腺腺样囊性癌细胞;促分裂原活化蛋白激酶;细胞凋亡

Abstract:

Abstract:Objective To explore the influence of icotinib in the apoptosis  of the human salivary adenoid cystic carcinoma cells ACC-M,and to clarify the mechanism of icotinib for the treatment of salivary adenoid cystic carcinoma.Methods The ACC-M cells were randomly divided into  controlgroup,2,4,8 μmo1/L-1 icotinib  groups,p38-MAPK inhibitor SB203580(20 μmol/L-1)   group, SB203580(20 μmol/L-1)+4 μmo1/L-1 icotinib  group;the cells were collected 4 h after treatment.The viability of ACC-M cells was measured by MTT assay.The apoptosis of ACC-M cells was assessed by caspase-3 activity kit.The expression of p-p38-MAPK protein was determined by Western blotting analysis.Results  Compared with control group,the  inhibitory rates of growth  of the ACC-M cells  in icotinib  groups  were significantly decreased(P<0.05),and the activities of caspase-3 were increased(P<0.05),and the expression levels  of p-p38-MAPK   were significantly increased(P<0.05).Compared with 4 μmo1?L-1 icotinib  group,the expression level of p-p38-MAPK in SB203580+icotinib  group were decreased(P<0.05),and the activity  of  caspase-3 was decreased dramatically (P<0.05).Conclusion Icotinib may induce the apoptosis of ACC-M cells through the activation of p38-MAPK signaling pathway.

Key words: icotinib, salivary adenoid cystic carcinoma cells, mitogen-activated protein kinase, apoptosis

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