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目的探讨甲基硒酸(methylseleninic acid,MSA)对紫杉醇治疗人三阴性乳腺癌(three negative breast cancer,TNBC)细胞的化疗增敏作用。方法分别采用MSA(4.5μmol/L)、紫杉醇(40 nmol/L)处理人乳腺癌细胞系MDA-MB-231(空白对照组:MSA-紫杉醇-;紫杉醇组:MSA-紫杉醇+;MSA组:MSA+紫杉醇-;联合用药组:MSA+紫杉醇+)。观察不同时间点MDA-MB-231细胞的体外增殖、细胞周期和细胞凋亡情况。结果 MSA组、紫杉醇组、联合用药组MDA-MB-231细胞的体外增殖抑制率、G1期细胞百分比、细胞凋亡率显著高于空白对照组(P<0.05),而各用药组的S期细胞百分比显著低于空白对照组(P<0.05),且上述作用均呈时间依赖性;不同时间条件下,联合用药组的体外增殖抑制率、G1期细胞百分比、细胞凋亡率显著高于空白对照组、紫杉醇组、MSA组(P<0.05),而MCF-7细胞的S期细胞百分比显著低于其他三组(P<0.05)。结论在MSA的增敏作用下,紫杉醇通过细胞周期G1/S阻滞效应抑制了MCF-7细胞的体外增殖,并强化了细胞凋亡诱导作用,更好地发挥对人TNBC的化疗治疗作用。
Objective To investigate the chemosensitivity of methylseleninic acid (MSA) to paclitaxel in three negative breast cancer (TNBC) cells. Methods The human breast cancer cell line MDA-MB-231 (blank control group: MSA-paclitaxel-; paclitaxel group: MSA-paclitaxel +; MSA group) was treated with 4.5μmol / L MSA and 40 nmol / MSA + paclitaxel -; combination group: MSA + paclitaxel +). The proliferation, cell cycle and apoptosis of MDA-MB-231 cells at different time points were observed. Results The proliferation inhibition rate, the percentage of cells in G1 phase and the apoptosis rate of MDA-MB-231 cells in MSA group, paclitaxel group and combination group were significantly higher than those in blank control group (P <0.05) The percentage of cells in G1 phase and the percentage of cells in G1 phase were significantly higher than those in blank control group (P <0.05), and the above effects were time-dependent. Under different time, Control group, paclitaxel group and MSA group (P <0.05), while the percentage of S phase cells in MCF-7 cells was significantly lower than the other three groups (P <0.05). Conclusions Under the sensitization of MSA, paclitaxel can inhibit the proliferation of MCF-7 cells in vitro through cell cycle G1 / S blockade, and enhance the induction of apoptosis and make better use of chemotherapeutic effect on human TNBC.