阿霉素对人乳腺癌细胞凋亡及去磷酸化RB 蛋白表达的影响

目的 探讨阿霉素(ADR) 体外诱导人乳腺癌化疗敏感细胞(MCF-7 S) 凋亡与去磷酸化RB 蛋白表达之间的关系。 方法 应用MTT 比色法检测ADR对体外培养的MCF-7 S 细胞增殖抑制作用, 同时应用末端标记(TUNEL) 法观测ADR 对MCF-7 S 细胞凋亡程度的影响。采用免疫细胞化学法检测去磷酸化RB 蛋白的表达水平。 结果 ADR 抑制MCF-7 S细胞增殖呈剂量依赖性, 半数抑制浓度(IC₅₀) 为0.128 mg·L^-1;ADR 作用组MCF-7 S 细胞的凋亡率(apoptotic rate, AR) 为0.261, 较对照组(0.045) 明显增高(P <0.01);ADR 作用组MCF-7 S 细胞的去磷酸化RB 蛋白表达量MOD(阳性细胞平均光密度) ×area(阳性面积相对比) 均数是987 ±207, 较对照组132 ±32 显著增高(P <0.01);ADR 能促进MCF-7 S细胞内去磷酸化RB 蛋白的表达。在ADR 作用组,MCF-7 S 细胞的凋亡率与去磷酸化RB 蛋白表达量呈正相关(P <0.05)。 结论 ADR 抑制MCF-7 S 细胞增殖和诱导MCF-7 S 细胞凋亡可能与细胞内去磷酸化RB 蛋白表达水平有关。

Effects of adriamycin on cell apoptosis and expression of dephosphorylated RB protein in human breast cancer

AIM: To investigate the roles that adriamycin (ADR) plays in the expression of dephosphorylated RB protein and inducing apoptosis of human breast cancer cells (MCF-7/S) cultured in vitro. METHODS: MTT colorimetric assay was applied to examine the growth inhibition, and apoptosis rates (AR) were determined by terminal-deoxynucleotidyl transferase mediated d-UTP nick end labeling (TUNEL);the expressive levels of dephosphorylated RB protein were detected with immunocytochemistry. RESULTS: ADR inhibited proliferation of MCF-7 S cells in a dose dependent manner, and the 50 % inhibition concentration (IC50) was 0.128 mg·L^-1.Tumor cell AR in ADR group ($x^{-}$=0.261) was significantly higher than that in control group ($x^{-}$=0.045, P < 0.01).The expressive levels of dephosphorylated RB protein in ADR group (MOD ×area=987 ±207) was significantly higher than that in control group (MOD ×area=132 ±32, P <0.01).The dephosphorylated RB was enhanced by ADR in breast cancer cells.There was significant positive correlation between AR and the expressive levels of dephosphorylated RB protein in ADR group (P <0.05). CONCLUSION: ADR inhibits the growth proliferation and induces apoptosis in MCF-7/S cell line, which is possibly related to enhancing dephosphorylated RB protein expression.