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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 investigate the role of calcium signaling in the proliferation of colon cancer SW620 cells induced by PAR2-AP. METHODS: SW620 cells were treated with 100 μmol / L PAR2-AP and the fluorescence intensity of intracellular Ca2 + was measured by fluo-4 / AM fluorescence assay. The concentration of EGTA was 1 mmol / L, The changes of phosphorylation of extracellular signal-regulated kinase 1/2 (p-ERK1 / 2) were detected by Western blot after pretreated with 100μmol / L PAR2 and 1μmol / L of TG and 1μmol / L of PAR2- Proliferation activity changes, cell cycle changes detected by flow cytometry. Results After SW220 cells were stimulated with PAR2-AP, the fluorescence intensity of Ca2 + increased transiently and then decreased. The cells pretreated with EGTA and TG significantly interfered the up-regulation of p-ERK1 / 2 and the cell proliferation by PAR2-AP. CONCLUSIONS: PAR2-AP activates PAR2 receptor and affects the expression of p-ERK1 / 2 via calcium signaling pathway and promotes the proliferation of SW620 cells.