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目的探讨锌原卟啉(ZnPP)对种植性乳腺癌细胞凋亡及信号传导和转录因子-3 (STAT-3)的影响。方法应用种植性乳腺癌模型,结合ZnPP、钴原卟啉(CoPP)处理,分别用逆转录-聚合酶链反应(RT-PCR)检测乳腺癌组织中的血红素氧合酶-1(HO-1)mRNA并HO-1酶活性, 免疫组织化学、Western blot蛋白印迹杂交检测癌组织中HO-1、CAS-3、bcl-XL、STAT-3蛋白表达。 TUNEL法评价肿瘤细胞凋亡。结果 ZnPP组肿瘤平均直径明显低于其余各组(t=3．632 4,P< 0．01);CoPP组最大(t=3．554 6,P<0．01)。ZnPP组肿瘤组织内的HO-1 mRNA、HO-1蛋白及HO- 1酶活性均低于其余各组,而CoPP组高于其余各组。ZnPP组STAT-3及bcl-XL蛋白表达低于 CoPP组(t=2．421 6,P<0．05)(t=4．370 6,P<0．01),CoPP+ZnPP组STAT-3高于空白对照组 (t=2．796 5,P<0．05),其余各组间差异无统计学意义(P>0．05)。ZnPP组CAS-3蛋白表达及肿瘤细胞凋亡指数与其他组相比较明显增高(t=3．685 6,P<0．01)(t=3．596 9,P<0．01)。结论 ZnPP可能通过抑制HO-1蛋白的表达来降低STAT-3和bcl-XL蛋白表达,从而增加CAS-3的表达,并可能由此增加了肿瘤细胞凋亡的发生。
Objective To investigate the effects of zinc protoporphyrin (ZnPP) on apoptosis and signal transduction and transcription factor-3 (STAT-3) in human breast cancer cells. Methods The model of breast cancer was established. Combined with ZnPP and CoPP treatment, the expression of HO-1 in breast cancer tissues was detected by reverse transcription-polymerase chain reaction (RT-PCR) 1) mRNA and HO-1 activity, immunohistochemistry and Western blot were used to detect the expression of HO-1, CAS-3, bcl-XL and STAT-3 in cancer tissue. TUNEL method to evaluate tumor cell apoptosis. Results The mean diameter of tumor in ZnPP group was significantly lower than that in the other groups (t = 3.632 4, P <0.01), and that in CoPP group was the highest (t = 3.554 6, P <0.01). The activity of HO-1 mRNA, HO-1 protein and HO-1 in ZnPP group were lower than those in other groups, while the CoPP group was higher than the other groups. The expressions of STAT-3 and bcl-XL in ZnPP group were lower than that in CoPP group (t = 2.421 6, P <0.05) (t = 4.370 6, P <0.01) 3 was higher than that in the blank control group (t = 2.796 5, P <0.05). There was no significant difference among the other groups (P> 0.05). The protein expression of CAS-3 and apoptosis index in ZnPP group were significantly higher than those in other groups (t = 3.685 6, P <0.01) (t = 3.596 9, P <0.01). Conclusion ZnPP may reduce the expression of STAT-3 and bcl-XL protein by inhibiting the expression of HO-1 protein, thereby increasing the expression of CAS-3 and possibly increasing the apoptosis of tumor cells.