薯蓣次苷A通过下调STAT3及糖代谢相关基因表达抑制MCF7细胞生长  

Prosapogenin A inhibits cell growth of MCF7 via downregulating STAT3 and glycometabolism-related gene

作　　者：王天晓[1] 时小燕[1] 丛悦[1] 张中庆[1] 刘迎滑[1] 

机构地区：[1]河南大学中药研究所,河南大学药学院,河南开封475004

出　　处：《药学学报》2013年第9期1510-1514,共5页Acta Pharmaceutica Sinica

基　　金：河南省科技厅重点攻关项目(122102310558);河南省教育厅自然科学研究项目(2011A310001)

摘　　要：肿瘤的发生和发展是一个复杂的过程,肿瘤细胞的失控性生长是肿瘤的重要生物学特征,而肿瘤细胞的快速生长则依赖于葡萄糖代谢提供能量ATP及代谢中间产物用于肿瘤细胞生物大分子的合成。正常组织细胞在有氧时通过糖的有氧分解获取能量,只有在缺氧时才进行无氧糖酵解。但肿瘤细胞即使在供氧充足的条件下,也主要依赖糖酵解进行代谢,肿瘤细胞的这种特性被称为Warburg效应。This study is to investigate the inhibitory effect and mechanism of prosapogenin A （PSA） on MCF7. MTT assay was performed to determine the inhibitory effect of PSA on MCF7 cells. PI/Hoechst 33342 double staining was used to detect cell apoptosis. RT-PCR was used to test the mRNA levels of STAT3, GLUT1, HK and PFKL. Western blotting was performed to determine the expression of STAT3 and pSTAT3 protein in MCF7 cells. The results showed that PSA could dose-dependently inhibit cell growth of MCF7 followed by ICs0 of 9.65 μmol·L^-1 and promote cell apoptosis of MCF7. Reduced mRNA levels of STAT3, HK and PFKL were observed in MCF7 cells treated with 5 μmol·L^-1 of PSA. PSA also decreased the level of pSTAT3 protein. STAT3 siRNA caused decrease of mRNA of GLUT1, HK and PFKL which indicated STAT3 could regulate the expressions of GLUT1, HK and PFKL. The results suggested that PSA could inhibit cell growth and promote cell apoptosis of MCF7 via inhibition of STAT3 and glycometabolism-related gene.

关 键 词：STAT3 糖代谢 细胞凋亡 MCF7细胞 

分 类 号：R963[医药卫生—微生物与生化药学]