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作 者:王静[1] 吴莺[1] 余小燕[1] 蒋双红[1] 胡丽超[2] 周红[2]
机构地区:[1]江苏大学附属医院消化病科,212013 [2]江苏大学基础医学与医学技术学院
出 处:《江苏医药》2013年第13期1492-1495,共4页Jiangsu Medical Journal
基 金:江苏省自然科学基金(BK2010336)
摘 要:目的探讨钙信号在蛋白酶活化受体2激动剂(PAR2-AP)促进结肠癌SW620细胞增殖中的作用。方法 PAR2-AP 100μmol/L作用于SW620细胞,用fluo-4/AM荧光法测定细胞内Ca2+荧光强度的变化;乙二醇-双-(2-氨基乙醚)四乙酸(EGTA)1mmol/L、毒胡萝卜内酯(TG)1μmol/L、PAR2-AP 100μmol/L预处理细胞后,Western blot检测磷酸化细胞外信号调节激酶1/2(p-ERK1/2)的变化,MTT法检测SW620细胞增殖活力的变化,流式细胞术检测细胞周期的变化。结果 PAR2-AP刺激SW620细胞后,Ca2+荧光强度短暂升高后减低;EGTA和TG预处理细胞能明显干预PAR2-AP对p-ERK1/2的升高作用及其促细胞增殖作用。结论 PAR2-AP活化PAR2受体后经钙信号通路影响p-ERK1/2表达,促进SW620细胞的增殖。Objective To elucidate the effects of calcium signaling on the proliferation of colon cancer SW620 cells induced by protease-activated receptor 2 agonists (PAR2-AP). Methods The SW620 cells were treated with PAR2-AP and the changes of intracellular Ca2+ concentration ([Ca2+]i) were detected with fluo-4/AM using confocal laser scanning microscopy. After the cells were pretreated with ethylene glycol tetraacetic acid (EGTA), thapsigargin and PAR2-AP, the expression of phosphorylated extracellular signal-regulated kinase 1/2 (p-ERK1/2), the proliferative potential of SW620 cells and the changes of cell cycle distribution were detected by Western blot, MTT and flow cytometry, respectively. Results [Ca2+ ]i was transiently elevated in SW620 cells after stimulated by PAR2-AP. The activation of p-ERK1/2 and the proliferation of SW620 cells induced by PAR2-AP could be inhibited by EGTA and thapsigargin pretreatment. Conclusion PAR2-dependent calcium signaling pathway is critical for activation of p-ERK1/2 and proliferation of SW620 cells induced by PAR2-AP.
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