摘要
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 effect of zinc protoporphyrin （ZnPP） on apotusis and STAT-3 in planted breast carcinoma. Methods The planted breast carcinoma was treated with ZnPP and cobalt protoporphyrin （CoPP）. The heme oxygenase-1（HO-1） mRNA and protein and enzyme activity in carcinoma tissue were assayed by RT-PCR and Western blot. At the same time CAS-3, bcl-XL, signal transducers and activators of transcription-3 （STAT-3） protein were examined by immunohistochemstery and Western blot and breast carcinoma cell apoptosis was stained by TUNEL. Results The diameter of tumor in ZnPP group was significantly smaller than that in other groups （ t = 3. 632 4, P 〈 0.01） and that in CoPP group was biggest （t = 3. 554 6, P 〈 0.01）. The HO-1 mRNA and protein and HO-1 enzyme activity in tumor of ZnPP group were lower than those in other groups, and those in CoPP group were highest. The expression of STAT-3 and bcl-XL protein in ZnPP group was lower than that in CoPP group （ t = 2. 421 6 P 〈 0.05） （ t = 4. 370 6, P 〈 0.01）, the STAT-3 protein in CoPP ＋ ZnPP group was higher than that in control group （ t = 2. 796 5, P 〈 0.05）, and no difference was found among other groups. The expression of CAS-3 protein and carcinoma cell apoptosis index in ZnPP group were significantly higher than those in control and CoPP ＋ ZnPP groups （t= 3.6856, P〈 0.01） （t= 3. 596 9, P〈 0.01）. Conclusion ZnPP is likely to decrease the expression of STAT-3 protein and bcl- XL protein by inhibiting the HO-1 protein expression, consequently increase the expression of CAS-3 and enhance the rate of breast carcinoma cell apoptosis.
出处
《中华实验外科杂志》
CAS
CSCD
北大核心
2006年第5期525-527,i0001,共4页
Chinese Journal of Experimental Surgery
