文献类型：期刊文献

英文题名：miR-149 regulates the proliferation and apoptosis of human colonic carcinoma cells by targeting FZD5

作者：Liu, Xiaozhu Li, Yinfeng Chen, Cuicui Li, Laiqing

第一作者：刘晓柱

通信作者：Liu, XZ[1]

机构：[1]Guizhou Inst Technol, Coll Food & Pharmaceut Engn, Guiyang 550003, Peoples R China;[2]Guangzhou Youdi Biotechnol Co Ltd, Guangzhou, Peoples R China

第一机构：贵州理工学院食品药品制造工程学院

通信机构：corresponding author), Guizhou Inst Technol, Coll Food & Pharmaceut Engn, Guiyang 550003, Peoples R China.|贵州理工学院食品药品制造工程学院;贵州理工学院;

年份：2020

卷号：13

期号：5

起止页码：889-895

外文期刊名：INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL PATHOLOGY

收录：;WOS:【SCI-EXPANDED(收录号:WOS:000537945000007)】；

基金：This work was supported by Guizhou Science and Technology Plan Project [(2018)1069].

语种：英文

外文关键词：miR-149; colorectal cancer (CRC); Frizzled class receptor 5 (FZD5); Wnt/beta-catenin signal pathway

摘要：Objective: To explore the effects of miR-149 on the cell proliferation and apoptosis of colorectal cancer (CRC) and its potential molecular mechanism. Methods: miR-149 expression patterns were detected in human CRC cell lines by quantitative real-time RT-PCR (Q-PCR). Online prediction software and luciferase reporter assay were performed to screen the functional targets of miR-149. CRC cells were transfected with miR-149 mimics or siRNAs of FZD5 and then divided into NC group (negative control), miR-149 mimics group (cells transfected with miR-149 mimics) and miR-149 mimics + SiFZD5 group (cells transfected by miR-149 mimics and SiFZD5). Moreover, the effects of miR-149 on the proliferation and apoptosis of CRC cells were also analyzed by MTT and flow cytometry assay. In addition, the expression of Wnt/beta-catenin signal pathways related factors were shown by western blot analysis. Results: Q-PCR results demonstrated that the expression of miR-149 was significantly lower in SW480 than that in the FHC cell line. Frizzled class receptor 5 (FZD5) was identified as a functional target of miR-149 through a series of experiments including Q-PCR, western blot analysis, and luciferase assay. Cellular functional experiments demonstrated that the cell viability and proliferation were greatly inhibited after miR-149 overexpression in SW480 cells. Furthermore, the proportion of apoptotic cells increased significantly after introducing miR-149 into SW480 cells. Furthermore, Wnt/beta-catenin signal pathway was activated because of the lower expression of beta-catenin and cyclinD1 in miR-149 mimics group. However, reducing FZD5 expression restored the expression of beta-catenin and cyclin D. Conclusions: Our data suggested that miR-149 may function as a tumor suppressor in CRC cells lines by targeting FZD5. miR-149/FZD5 may become a new therapeutic target for CRC.