| p38^MAPK对卵巢癌顺铂耐药作用及机制的探讨 |
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| 引用本文： | 焦今文,赵新卫,邓博雅,庞晓燕,温放. p38^MAPK对卵巢癌顺铂耐药作用及机制的探讨[J]. 齐鲁肿瘤杂志, 2012, 0(16): 1221-1226 |
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| 作者姓名： | 焦今文 赵新卫 邓博雅 庞晓燕 温放 |
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| 作者单位： | [1]青岛大学医学院附属医院妇科,山东青岛266000 [2]青岛经济技术开发区第一人民医院骨三科,山东青岛266000 [3]中国医科大学附属第一医院妇科,辽宁沈阳110001 |
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| 摘 要： | 目的：研究p38^MAPK在卵巢上皮癌顺铂化疗耐药中的作用，并探讨其作用机制。方法：蛋白质印迹法检测顺铂对卵巢癌中p38^MAPK的激活情况；MTT法检测p38^MAPK抑制荆SB203580处理后及p38shRNA干扰后细胞顺铂耐药指数的变化；实时定量PCR技术检测SB203580处理后及p38shRNA干扰后，耐药蛋白ERCCl、MDR、LRP、GST-π及凋亡蛋白Caspase3、Survivin等mRNA的表达变化。结果：在=定时间浓度梯度下，顺铂可诱导卵巢癌顺铂敏感株COCl及耐药株COC1／DDP细胞内p38^MAPK的激活，但耐药株的激活程度弱于敏感株；p38^MAPK抑制剂SB203580及p38shRNA干扰可增加卵巢癌细胞株的耐药指数（t=4．610，P=0．041；t=11．621，P=0．000）；SB203580及p38shRNA干扰后SurvivinmRNA（f=5．152，P=0．007；t=6．008，P=0．004）、ERCClmRNA（t=13．742，P=0．005；t=11．621，P=0．000）及LRPmRNA（t=8．173，P=0．001；￡=16．815，P=0．000）的表达明显上调。结论：p38^MAPK受抑制可能导致卵巢上皮性癌顺铂耐药的产生，其机制可能是通过上调Survivin、ERCC1及LRP的mRNA表达来实现。
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| 关 键 词： | 卵巢肿瘤 p38^MAPK 抗药性 多药 印迹法 蛋白质 |
Role of the p38^MAPK pathway in cisplatin resistant ovarian cancer and its mechanism |
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| JIAO Jin-wen,ZHAO Xin-wei,DENG Bo-ya,PANG Xiao-yan,WEN Fang. Role of the p38^MAPK pathway in cisplatin resistant ovarian cancer and its mechanism[J]. , 2012, 0(16): 1221-1226 |
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| Authors: | JIAO Jin-wen ZHAO Xin-wei DENG Bo-ya PANG Xiao-yan WEN Fang |
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| Affiliation: | 1. Department of Gynecology ,Affiliated Hospital ,Medical College Qingdao University ,Qingdao 266000 ,P. R. China 2. Third Department of Orthopaedics, First People＇s Hospital ,Qingdao Economic and Techndogical Development Are a ,Qingdao 266000 ,P. R. China 3. Department of Gynecology, First Affiliated Hospital, China Medical University, Shenyang 110001, P. R. China |
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| Abstract: | OBJECTIVE：To investigate the role of p38MAPK in cisplatin resistant ovarian cancer and to explore its mecha- nism. METHODS： Using Western blot to detect the activation of p38MApK in ovarian cancer treated with cisplatin;Using MTT assay to detect the change of cisplatin resistant index after adding p38^MAPK inhibitor SB203580 or disturbed by p38^MAPK Real- time quantitative PCR was used to detect the change of resistance protein ERCCl, MDR, LRP, GST-n and the apoptotic protein Caspase-3,Survivin mRNA＇s after adding p38^MAPK inhibitor SB203580 or disturbed by p38^MAPK. RESULTS.. At a certain time/concentration gradient, eisplatin could activate p38MApK both in ovarian cancer cisplatin-sensitive line COCl and cisplatin-re- sistant line COCl/DDP cell but the activation level of COCl/DDP cell was weaker;SB203580 and p38^MAPK could increse the RI（Resistant Index） of ovarian cancer cell lines （t = 4.610, P = 0.041 ; t= 11.621, P = 0. 000） Survivin mRNA （t = 5.152, P = 0.007;t 6.008,P=0.004）,ERCCl mRNA （t=13.742,P=0.005;t=11.621,P=0.000）and LRPrnRNA（t=8.173,P= 0.001 ; t = 16.815, P = 0.000） were significantly upregulated aft er treating with SB203580 or p38^MAPK. CONCLUSION ： Inhi- bition of p38MAPK may result in cisplatin resistance in epithelial ovarian cancer cells and it is probably caused by the up-regulation of the mRNA expression of Survivin,ERCCl and LRP. |
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| Keywords: | ovarian neoplasms p38MAPK drug resistance, multiple blotting, western |
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