Formononetin inhibits human bladder cancer cell proliferation and invasiveness via regulation of miR-21 and PTEN
Formononetin inhibits human bladder cancer cell proliferation and invasiveness via regulation of miR-21 and PTEN
复制标题
芒柄花素通过调节 miR-21 和 PTEN 抑制人膀胱癌细胞增殖和侵袭
DOI：
10.1039/c6fo01535b
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发表时间：
2017-03-01
期刊：
影响因子：
6.1
通讯作者：
Li, Tianyu
中科院分区：
文献类型：
--
作者：
Wu, Yiying;Zhang, Xing;Li, Tianyu
异黄酮芒柄花素是黄芪的主要活性成分，具有抗肿瘤作用。然而，刺芒柄花素在人膀胱癌（BCa）中的作用尚未完全阐明。本研究旨在探讨芒柄花素对BCa细胞的抗肿瘤作用及其可能的分子机制。用不同浓度的芒柄花素处理T24细胞，MTT法检测细胞增殖，Hoechst 33258染色法检测细胞凋亡，transwell侵袭法检测细胞侵袭性，real-time PCR检测microRNA-21 （miR-21）表达，western blotting检测磷酸酶和张力素同源物（PTEN）及磷酸化Akt同源物（p-Akt）蛋白水平。结果表明，刺芒柄花素对T24细胞的增殖具有明显的抑制作用，且具有时间和剂量依赖性。刺芒柄花素对T24细胞有明显的凋亡形态学改变，侵袭性降低。此外，在刺芒柄花素处理的T24细胞中，miR-21的表达显著降低，随后PTEN升高，p-Akt下调。综上所述，这些结果表明芒柄花素在体外对BCa具有抗癌作用，这可能是由于mir -21介导的PTEN/Akt通路的调控。
The isoflavone formononetin is the main active component of Astragalus membranaceus and possesses anti-tumorigenic properties. However, the role of formononetin in human bladder cancer (BCa) has not been fully elucidated. The aim of the present study was to investigate the anti-tumor effects of formononetin on BCa cells and its potential molecular mechanism. T24 cells were treated with different concentrations of formononetin, and then the cell proliferation was assessed by MTT assay, cell apoptosis by Hoechst 33258 stain assay, cell invasiveness by transwell invasion assay, microRNA-21 (miR-21) expression by real-time PCR and the protein level of phosphatase and tensin homolog (PTEN) and phosphorylated homolog of Akt (p-Akt) by western blotting. The results showed that formononetin significantly inhibited the proliferation of T24 cells in a time-and dose-dependent manner. T24 cells treated with formononetin displayed obvious morphological changes of apoptosis and lower invasiveness. In addition, miR-21 expression was significantly decreased in formononetin-treated T24 cells, followed by increase of PTEN, and down-regulation of p-Akt. Collectively, these results suggest that formononetin exerts an anti-carcinogenic effect on BCa in vitro, which might be due to miR-21-mediated regulation of the PTEN/Akt pathway.