
MeCP2 inhibits proliferation and migration of breast cancer via suppression of epithelial‐mesenchymal transition
Author(s) -
Jiang Wei,
Liang YanLing,
Liu Yang,
Chen YuYan,
Yang ShuTing,
Li BiRong,
Yu YingXian,
Lyu Yansi,
Wang Rikang
Publication year - 2020
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.15428
Subject(s) - mecp2 , epithelial–mesenchymal transition , cancer research , gene knockdown , cell growth , epigenetics , breast cancer , biology , cell migration , cancer , pathology , cell , metastasis , medicine , cell culture , phenotype , biochemistry , genetics , gene
Methyl‐CpG‐binding protein 2 (MeCP2) is an important epigenetic regulator for normal neuronal maturation and brain glial cell function. Additionally, MeCP2 is also involved in a variety of cancers, such as breast, prostate, lung, liver and colorectal. However, whether MeCP2 contributes to the progression of breast cancer remains unknown. In the present study, we investigated the role of MeCP2 in cell proliferation, migration and invasion in vitro. We found that knockdown of MeCP2 inhibited expression of epithelial‐mesenchymal transition (EMT)‐related markers in breast cancer cell lines. In conclusion, our study suggests that MeCP2 inhibits proliferation and invasion through suppression of the EMT pathway in breast cancer.