芒柄花苷的体外抗乳腺癌作用及机制研究

目的研究芒柄花苷对乳腺癌细胞MCF-7增殖、凋亡和侵袭的影响及作用机制。方法采用不同浓度芒柄花苷处理乳腺癌细胞MCF-7,噻唑盐(MTS)染色检测细胞活力,Ed U检测细胞增殖能力,Hoechst染色法检测细胞凋亡,Transwell小室实验检测细胞侵袭和迁移能力,Western-blotting检测增殖细胞核抗原(PCNA)、凋亡相关蛋白(Bax和Bcl-2)和基质蛋白酶(MMP)-9的表达。结果芒柄花苷剂量和时间依赖性的抑制MCF-7细胞的生长。MCF-7细胞经芒柄花苷干预后,Ed U阳性细胞数减少、侵袭及迁移细胞数减少和Hoechst阳性细胞数增加。芒柄花苷作用MCF-7细胞,可上调Bax的表达和下调Bcl-2、PCNA和MMP-9的表达。结论芒柄花苷可抑制乳腺癌细胞MCF-7的增殖、诱导凋亡和减少侵袭,其机制可能分别涉及调节PCNA、Bcl-2/Bax和MMP-9的表达。

Anti-breast Cancer Effect of Ononin and Its Mechanism in Vitro

OBJECTIVE To investigate the anti-breast cancer effect of ononin and its mechanism in vitro. METHODS After treating with different concentration of ononin,the MCF-7 cells viability was determined by MTS,Ed U and Hoechst were used to measure the proliferative ability and apoptotic rate of MCF-7,respectively. The invasion and migration of MCF-7 were determined by Transwell assays. The protein expression including PCNA,apoptosis-related proteins( Bax and Bcl-2) and MMP-9 were evaluated by Western-blotting. RESULTS Ononin inhibited the cells viability of MCF-7 in a dose-and time-dependent manner. The Ed U positive cells were decreased,Hoechst positive cells were increased,invasive and migration cells were decreased after treating with ononin in MCF-7. Moreover,ononin up-regulated Bax expression and down-regulated Bcl-2,PCNA as well as MMP-9 expression. CONCLUSION Ononin could inhibit the MCF-7 cells proliferation,promote cells apoptosis,decrease cells invasion and migration,which may involve the regulative effect on PCNA,Bax/Bcl-2 and MMP-9 expression.