中国现代医学杂志2016，Vol.26Issue(24)：18-23,6.DOI:10.3969/j.issn.1005-8982.2016.24.004
姜黄素通过下调microRNA-211表达促进结肠癌细胞的凋亡及其机制
Curcumin promotes apoptosis in colon cancer by downregulating miR-211 expression
武嘉庚1
作者信息
- 1. 青海省药品检验检测院 藏药室，青海 西宁 810000
- 折叠
摘要
Abstract
Objective To study the effect of curcumin on miR-211 in colon cancer cells and clarify a miR-211-mediated mechanism which plays a role in the anti-tumor effects of curcumin. Methods The dose-effect and time-effect relationship of curcumin on HCT116 was tested by MTT assay and flow cytometry. Expression level of miR-211 in curcumin-treated HCT116 was detected by qRT-PCR. TP53INP1 was predicted as a target of miR-211 using GeneTarget database and confirmed by dual luciferase reporter assays. Additionally, the effect of upregulating miR-211 by miR-211 mimics or silencing TP53INP1 by siRNA on curcumin-treated HCT116 was examed by MTT and flow cytometry. Results Compared with untreated HCT116 cells, curcumin at 10-50 μmol/L inhibited cell proliferation and induced apoptosis in a dose-dependent and time-dependent manner. Curcumin also produced a dose and time dependent suppression of miR-211 ( < 0.05). Moreover, the protein level of TP53INP1 was significantly elevated in crucumin-treated HCT116 cells ( <0.05). Transfection of HCT116 with miR-211 mimics or TP53INP1 small interfering RNA significantly reversed the effect of curcumin on HCT116, compared to corresponding controls ( <0.05). Conclusions Our data suggest a novel molecular mechanism in which inhibition of miR-211 and upregulation of TP53INP1 mediate the anticancer activities of curcumin in colon cancer cells.关键词
结肠癌/miR-211/姜黄素/TP53INP1/凋亡Key words
colon cancer/miR-211/curcumin/TP53INP1/apoptosis分类
医药卫生引用本文复制引用
武嘉庚..姜黄素通过下调microRNA-211表达促进结肠癌细胞的凋亡及其机制[J].中国现代医学杂志,2016,26(24):18-23,6.
