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目的:研究6,8-二-三氟甲基-7-乙酰氧基白杨素(9dFMAChR))抑制体外培养人卵巢癌细胞系CoC1细胞增殖和诱导凋亡作用及机制。方法:体外培养CoC1细胞,MTT比色法测定dFMAChR对CoC1细胞增殖活性的影响;AO/EB染色法荧光显微镜观察dFMAChR诱导CoC1凋亡细胞的形态学改变;DNA凝胶电泳确证dFMAChR诱导CoC1细胞凋亡作用;Western blotting法分析dFMAChR对CoC1细胞酪蛋白激酶CK2α蛋白表达和活性的影响。结果:MTT比色法结果显示,dFMAChR有效抑制CoC1细胞增殖活性,呈剂量依赖性;其IC50值为11.8μM。AO/EB染色荧光显微镜观察dFMAChR处理后,部分CoC1细胞呈现典型凋亡细胞形态特征;dFMAChR(10.0μM)处理CoC1细胞48 h,琼脂糖凝胶电泳出现“梯形”DNA条带。Western blotting分析结果表明:dFMAChR下调酪蛋白激酶CK2α表达,呈浓度和时间依赖性。结论:dFMAChR具有抑制人卵巢癌CoC1细胞增殖和诱导细胞凋亡作用;作用机制与其抑制酪蛋白激酶CK2α表达有关。
AIM: To investigate the effects of 6,8-bis-trifluoromethyl-7-acetoxychitosan (9dFMAChR) on proliferation and apoptosis of human ovarian cancer cell line CoC1 in vitro and its mechanism. Methods: CoC1 cells were cultured in vitro. The effect of dFMAChR on the proliferation of CoC1 cells was measured by MTT colorimetric assay. The morphological changes of CoC1 cells were observed by AO / EB staining with fluorescence microscopy. DNA gel electrophoresis confirmed that dFMAChR induced CoF1 cells apoptosis The effect of dFMAChR on the protein expression and activity of casein kinase CK2α in CoC1 cells was analyzed by Western blotting. Results: MTT assay showed that dFMAChR effectively inhibited the proliferation of CoC1 cells in a dose-dependent manner with an IC50 value of 11.8 μM. After treated with dFMAChR by AO / EB staining, some of the CoC1 cells showed morphological features of typical apoptotic cells; CoC1 cells were treated with dFMAChR (10.0μM) for 48 h and “trapezoidal” DNA bands were observed by agarose gel electrophoresis. Western blotting analysis showed that dFMAChR down-regulated the expression of casein kinase CK2α in a time-and concentration-dependent manner. CONCLUSION: dFMAChR can inhibit the proliferation and induce the apoptosis of human ovarian cancer CoC1 cells. Its mechanism is related to its inhibition of the expression of casein kinase CK2α.