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全反式维甲酸对人胃腺癌细胞中Akt及其磷酸化蛋白表达的影响
引用本文:杨艳梅,张春艳,马玉彦,杨悦,任丽君,秦莉,袁玉涛.全反式维甲酸对人胃腺癌细胞中Akt及其磷酸化蛋白表达的影响[J].实用肿瘤学杂志,2010,24(3):209-211,223.
作者姓名:杨艳梅  张春艳  马玉彦  杨悦  任丽君  秦莉  袁玉涛
作者单位:哈尔滨医科大学肿瘤研究所,哈尔滨,150081
基金项目:黑龙江省教育厅资助课题 
摘    要:目的研究全反式维甲酸(alltrans-retinoic acid,ATRA)对人胃腺癌细胞(SGC-7901)中Akt及其磷酸化蛋白p—Akt(Ser473)和p—Akt(Thr308)表达的影响及其对细胞凋亡的诱导作用。方法采用四甲基偶氮唑盐(MTT)方法检测ATRA对SGC-7901增殖的抑制作用;荧光混微镜观察细胞凋亡形态;Western blot方法检测不同浓度ATRA处理后的SGC-7901细胞中Akt、p-Akt(Ser473)和p-Akt(Thr308)的表达情况。结果ATRA对SGC-7901细胞增殖的抑制作用呈时间和剂量依赖性;ATRA处理48h时,荧光显微镜观察细胞呈现明显的凋亡形态学改变;Western blot检测显示ATRA对细胞中Akt蛋白的表达没有明显影响,但显著下调两种p-Akt蛋白的表达。结论ATRA诱导SGC~7901细胞凋亡可能与其抑制磷酸化Akt蛋白表达有关。

关 键 词:全反式维甲酸  胃癌  Akt

Effects of all trans-retinoic acid on the expression of Akt and P-Akts in human gastric carcinoma cell line
YANG Yanmei,ZHANG Chunyan,MA Yuyan,YANG Yue,REN Lijun,QIN Li,YUAN Yutao.Effects of all trans-retinoic acid on the expression of Akt and P-Akts in human gastric carcinoma cell line[J].Journal of Practical Oncology,2010,24(3):209-211,223.
Authors:YANG Yanmei  ZHANG Chunyan  MA Yuyan  YANG Yue  REN Lijun  QIN Li  YUAN Yutao
Institution:(Harbin Medical University Cancer Research Institute,Harbin 150081)
Abstract:Objective To investigate the effeets of all trans -retinoic acid( ATRA) on the expression of Akt or its phosphorylated proteins and on apoptosis of human gastric carcinoma cell line( SGC -7901 ). Methods The effects of ATRA on the cell proliferation was measured by methyl thiazolyl tetrazolium(MTT) ,the apoptosis of ATRA on SGC- 7901cells was observed by fluorescentmieroscope, and the expression of Akt, p- Akt ( Ser473 ) and p - Akt ( Thr308 ) were measured by Western blot. Results ATRA inhibits the proliferation of SGC -7901 cells in a dose and time dependent manner. SGC -7901 cells showing typical apoptosis morphological changes were induced by ATRA at 48 h. ATRA did not influence the expression of Akt, but significantly decreased the expression of p - Akt ( Ser473 ) and p - Akt( Thr308 ). Conclution ATRA could induce apoptosis by down - regulating expression of p - Akt( Ser473 ) and p - Akt( Thr308 ).
Keywords:Akt
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