Downregulation of FOXP2 promotes breast cancer migration and invasion through TGFβ/SMAD signaling pathway

Cancer metastasis and relapse are the primary cause of mortality for patients with breast cancer. The present study performed quantitative proteomic analysis on the differentially expressed proteins between highly metastatic breast cancer cells and parental cells. It was revealed that forkhead box P...

Full description

Saved in:
Bibliographic Details
Published in:Oncology letters 2018-06, Vol.15 (6), p.8582-8588
Main Authors: Chen, Meng-Ting, Sun, He-Fen, Li, Liang-Dong, Zhao, Yang, Yang, Li-Peng, Gao, Shui-Ping, Jin, Wei
Format: Article
Language:English
Subjects:
Bone cancer
Breast cancer
Cell cycle
Gastric cancer
Gene expression
Lymphatic system
Medical diagnosis
Metastasis
Oncology
Studies
Transcription factors
Citations: Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Cancer metastasis and relapse are the primary cause of mortality for patients with breast cancer. The present study performed quantitative proteomic analysis on the differentially expressed proteins between highly metastatic breast cancer cells and parental cells. It was revealed that forkhead box P2 (FOXP2), a transcription factor in neural development, may become a potential inhibitor of breast cancer metastasis. The results demonstrated that patients with a lower level of FOXP2 expression had significantly poorer relapse-free survival (P=0.0047). The transcription of FOXP2 was also significantly downregulated in breast cancer tissue compared with normal breast tissue (P=0.0005). In addition, FOXP2 may inhibit breast cancer cell migration and invasion . It was also revealed that the underlying mechanism may include the epithelial-mesenchymal transition process driven by the tumor growth factor β/SMAD signaling pathway. In conclusion, the present study identified FOXP2 as a novel suppressor and prognostic marker of breast cancer metastasis. These results may provide further insight into breast cancer prevention and the development of novel treatments.
ISSN:1792-1074
1792-1082
DOI:10.3892/ol.2018.8402