MicroRNA‑195 suppresses rectal cancer growth and metastasis via regulation of the PI3K/AKT signaling pathway

MicroRNA-195 通过调节 PI3K/AKT 信号通路抑制直肠癌的生长和转移

阅读:5
作者:Yeli Wang, Linsong Mu, Miaoling Huang

Abstract

MicroRNAs (miRNAs) play a vital role in the progression of cancer, however, only limited data on miRNAs in rectal cancer are available. The aim of the present study was to investigate whether miR‑195 could inhibit the progression of rectal cancer. The miR‑195 mimic was transfected into 2 types of human rectal cancer cells (SW837 and SW1463). Cell viability and apoptosis were analyzed by Cell Counting Kit‑8 (CCK‑8) assay and flow cytometry, and cell migration and invasion were assessed by scratch test and Transwell assay. The results revealed that insulin‑like growth factor 1 (IGF1) was predicted as a potential target of miR‑195 by Targetscan7.2, and the result was verified by dual‑luciferase reporter assay. The co‑transfection of IGF1 was performed to confirm the underlying mechanism of tumor suppressor of miR‑195 in rectal cancer. The activation of PI3K/AKT signaling was determined by western blotting. The levels of miR‑195 in SW837 and SW1463 cells were revealed to be lower than in human rectal mucosa epithelial cells. After the transfection with miR‑195, the cell viability was decreased, while the apoptosis was significantly increased (SW837: 5.21% vs. 20.96%; SW1463: 4.19% vs. 25.22%). Moreover, cell migration and invasion were significantly inhibited in the mimic group. miR‑195 specifically targeted IGF1, however, the co‑transfection of IGF1 could partially reverse the inhibitory effects of miR‑195 on rectal cancer cells. It was also determined that the phosphorylation of PI3K and AKT were significantly inhibited in the mimic group. The tumor suppressive ability of miR‑195 in rectal cancer cell proliferation and metastasis was mediated by blocking IGF1 expression and inhibiting the PI3K/AKT pathway.

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。