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作 者:温峰[1] 杨文发[1] 杨光天[1] 赵海岩[1] 薛鹏[1] 蔡成宽[1] 王鲲鹏[1] 方毅[1]
机构地区:[1]徐州医学院附属连云港医院泌尿外科,江苏省222002
出 处:《江苏医药》2013年第23期2810-2813,F0002,共5页Jiangsu Medical Journal
摘 要:目的探讨8-氯-环磷酸腺苷(8-Cl-cAMP)及其代谢物8-氯-腺苷(8-Cl-adenosine)靶向蛋白激酶A RⅠα(PKA RⅠα)抑制PC3M肿瘤生长的作用。方法采用MTT法检测PC3M细胞增殖;TUNEL法检测细胞凋亡;Western blot检测RⅠα、RⅡβ、Caspase-3、Bcl-2、p38丝裂原活化蛋白激酶(MAPK)和磷酸化p38 MAPK表达。结果 8-Cl-cAMP和8-Cl-adenosine抑制PC3M细胞生长(P<0.05),引起细胞凋亡(P<0.05),下调RⅠα表达,上调RⅡβ表达,激活磷酸化p38 MAPK,抑制Caspase-3和Bcl-2表达。结论 8-Cl-cAMP及其代谢物8-Cl-adenosine靶向PKA RIα抑制PC3M肿瘤生长。其机制可能通过cAMP/PKA通路激活MAPK通路起作用。Objective To investigate the effect of selective cAMP analogue on cell growth of androgen-independent prostate cancer. Methods PC3M cell proliferation was examined by MTT assay,PC3M cell apoptosis was examined by TUNEL assay, and the expressions of RIa, RIll3, Caspase-3,Bcl-2,p38 .MAPK and phospho-p38 MAPK were detected by Western blot. Results The 8-CI-cAMP and 8-Cl-adenosine inhibited PC3M cell growth(P^0. 05), induced apoptosis(P^0. 05), downlregulated R I a expression, upregulated R]~ ~ expression, activated phospho-p38 MAPK, and inhibited the expressions of Caspase-3 and Bcl-2. Conclusion C1-CAMP and its rnetabolite 8-Cl-adenosine-targeted PKA RIa inhibit the growth of PC3M tumor. The mechanism for this may be through MAPK pathway activated by cAMP/PKA pathway.
关 键 词:前列腺癌 环磷酸腺苷类似物 丝裂原活化蛋白激酶通路
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