Author
Listed:
- Chang Gong
(Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Medical Research Center
Breast Tumor Center, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University)
- Shaohua Qu
(Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Medical Research Center
Breast Tumor Center, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University)
- Xiao-Bin Lv
(Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Medical Research Center
Breast Tumor Center, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University)
- Bodu Liu
(Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Medical Research Center
Breast Tumor Center, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University)
- Weige Tan
(Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Medical Research Center
Breast Tumor Center, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University)
- Yan Nie
(Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Medical Research Center
Breast Tumor Center, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University)
- Fengxi Su
(Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Medical Research Center
Breast Tumor Center, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University)
- Qiang Liu
(Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Medical Research Center
Breast Tumor Center, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University)
- Herui Yao
(Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Medical Research Center
Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University)
- Erwei Song
(Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Medical Research Center
Breast Tumor Center, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University)
Abstract
BRMS1L (breast cancer metastasis suppressor 1 like, BRMS1-like) is a component of Sin3A–histone deacetylase (HDAC) co-repressor complex that suppresses target gene transcription. Here we show that reduced BRMS1L in breast cancer tissues is associated with metastasis and poor patient survival. Functionally, BRMS1L inhibits breast cancer cells migration and invasion by inhibiting epithelial–mesenchymal transition. These effects are mediated by epigenetic silencing of FZD10, a receptor for Wnt signalling, through HDAC1 recruitment and histone H3K9 deacetylation at the promoter. Consequently, BRMS1L-induced FZD10 silencing inhibits aberrant activation of WNT3-FZD10-β-catenin signalling. Furthermore, BRMS1L is a target of miR-106b and miR-106b upregulation leads to BRMS1L reduction in breast cancer cells. RNA interference-mediated silencing of BRMS1L expression promotes metastasis of breast cancer xenografts in immunocompromised mice, whereas ectopic BRMS1L expression inhibits metastasis. Therefore, BRMS1L provides an epigenetic regulation of Wnt signalling in breast cancer cells and acts as a breast cancer metastasis suppressor.
Suggested Citation
Chang Gong & Shaohua Qu & Xiao-Bin Lv & Bodu Liu & Weige Tan & Yan Nie & Fengxi Su & Qiang Liu & Herui Yao & Erwei Song, 2014.
"BRMS1L suppresses breast cancer metastasis by inducing epigenetic silence of FZD10,"
Nature Communications, Nature, vol. 5(1), pages 1-15, December.
Handle:
RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms6406
DOI: 10.1038/ncomms6406
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