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目的:探讨吉西他滨诱导胰腺癌细胞ABCG2的表达及与其化疗耐药的关系。方法:吉西他滨不同浓度、不同时间作用胰腺癌SW1990细胞后,用CCK-8法检测细胞的增殖抑制率,并计算吉西他滨不同作用时间的半数抑制浓度(IC50);根据IC50值选择合适浓度的吉西他滨,作用SW1990细胞24、48、72 h后,用流式细胞仪检测细胞凋亡率,并用Western blot和RT-PCR法检测ABCG2蛋白与mRNA的表达。结果:吉西他滨作用后,SW1990细胞增殖明显抑制,并呈浓度与时间依赖性,但IC50值呈时间依赖性增加(均P<0.05);3.9 mg/mL吉西他滨作用24、48、72 h后,SW1990细胞总凋亡率逐渐增加,但晚期凋亡率呈降低趋势,ABCG2蛋白与mRNA的表达明显升高,并呈时间依赖性(均P<0.05)。结论:吉西他滨能抑制胰腺癌细胞SW1990的增殖,但作用呈时间依赖性减弱,这可能与其诱导ABCG2上调表达有关。
Objective: To investigate the expression of ABCG2 induced by gemcitabine and its relationship with chemoresistance in pancreatic cancer cells. Methods: After treated with different concentrations of gemcitabine for different time periods, the inhibitory rates of proliferation of SW1990 cells were determined by CCK-8 assay, and the IC50 of gemcitabine was calculated. The optimal concentration of gemcitabine was determined by IC50. After treated with SW1990 for 24,48 and 72 h, the apoptosis rate of SW1990 cells was detected by flow cytometry. The expression of ABCG2 protein and mRNA was detected by Western blot and RT-PCR. Results: After gemcitabine treatment, the proliferation of SW1990 cells was significantly inhibited and in a concentration-dependent and time-dependent manner, but the IC50 increased in a time-dependent manner (all P <0.05). After gemcitabine administration of 3.9 mg / mL for 24,48 and 72 h, SW1990 The total apoptosis rate increased gradually, but the rate of late apoptosis decreased. The expression of ABCG2 protein and mRNA was significantly increased in a time - dependent manner (all P <0.05). Conclusion: Gemcitabine can inhibit the proliferation of pancreatic cancer cell line SW1990 in a time-dependent manner, which may be related to the up-regulation of ABCG2 expression.