miR‑200b‑3p inhibits proliferation and induces apoptosis in colorectal cancer by targeting Wnt1

miR-200b-3p 通过靶向 Wnt1 抑制结直肠癌增殖并诱导细胞凋亡

阅读:5
作者:Lijuan Chen, Xiangqun Wang, Yunhua Zhu, Jian Zhu, Qingzhong Lai

Abstract

MicroRNA (miR)‑200b‑3p is downregulated in multiple human cancer types. Wnt signaling serves a role in human colorectal cancer (CRC). The present study aimed to examine the effect of miR‑200b‑3p on human CRC and its potential association with Wnt signaling. The Cell Counting Kit‑8 (CCK‑8) was employed to assess cell viability. A flow cytometric assay was conducted to examine cell proliferation and apoptosis. The regulation model of miR‑200b‑3p and Wnt1 was assessed by a luciferase reporter assay. A commercial kit was used to evaluate the activity of caspase‑3 following treatment of the cells by miR‑200b‑3p or Wnt1. The expression of target factors was determined by a quantitative real‑time polymerase chain reaction and western blot analysis. The expression of miR‑200b‑3p was decreased in human CRC tissues and in cell lines. The bioinformatics analysis and the luciferase reporter assay revealed that Wnt1 may be a direct target of miR‑200b‑3p. Moreover, the viability and proliferation of CRC cells was suppressed by miR‑200b‑3p. miR‑200b‑3p additionally induced apoptosis in CRC cells. Furthermore, the caspase‑3 activity was enhanced in the miR‑200b‑3p mimics group. The expression of antigen Ki‑67 (additionally termed KI‑67) and β‑catenin was decreased, while the expression of cleaved caspase‑3 was increased by miR‑200b‑3p. In conclusion, miR‑200b‑3p inhibited proliferation and induced apoptosis in CRC cells by inactivating Wnt/β‑catenin signaling. The present study provided potential biomarkers and candidate modalities for the management of CRC.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。