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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | He, Rui Kong, Peng-zhou Tian, Hong-pan Lun, Shu-min Wang, Qing-shan Li, Xiao-qing Huang, Huan-jing Feng, Yu-mei |
| Description | Author Affiliation: Tian HP ( From the Department of Biochemistry and Molecular Biology and.); Lun SM ( From the Department of Biochemistry and Molecular Biology and.); Huang HJ ( From the Department of Biochemistry and Molecular Biology and.); He R ( From the Department of Biochemistry and Molecular Biology and.); Kong PZ ( From the Department of Biochemistry and Molecular Biology and.); Wang QS ( From the Department of Biochemistry and Molecular Biology and the Key Laboratory of Breast Cancer Prevention and Treatment of the Ministry of Education, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center of Cancer, Tianjin 300060, China.); Li XQ ( From the Department of Biochemistry and Molecular Biology and the Key Laboratory of Breast Cancer Prevention and Treatment of the Ministry of Education, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center of Cancer, Tianjin 300060, China.); Feng YM ( From the Department of Biochemistry and Molecular Biology and the Key Laboratory of Breast Cancer Prevention and Treatment of the Ministry of Education, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center of Cancer, Tianjin 300060, China ymfeng@tijmu.edu.cn.) |
| Abstract | FOXF2 (forkhead box F2) is a mesenchyme-specific transcription factor that plays a critical role in tissue homeostasis through the maintenance of epithelial polarity. In a previous study, we demonstrated that FOXF2 is specifically expressed in basal-like breast cancer (BLBC) cells and functions as an epithelial-mesenchymal transition suppressor. FOXF2 deficiency enhances the metastatic ability of BLBC cells through activation of the epithelial-mesenchymal transition program, but reduces cell proliferation. In this study, we demonstrate that CpG island methylation of the FOXF2 proximal promoter region is involved in the regulatory mechanism of the subtype-specific expression of FOXF2 in breast cancer cells. DNMT1, DNMT3A, and DNMT3B commonly or individually contributed to this DNA methylation in different breast cancer cells. SP1 regulated the transcriptional activity of FOXF2 through direct binding to the proximal promoter region, whereas this binding was abrogated through DNA methylation. FOXF2 mediated the SP1-regulated suppression of progression and promotion of proliferation of non-methylated BLBC cells. Thus, we conclude that the subtype-specific expression and function of FOXF2 in breast cancer cells are regulated through the combined effects of DNA methylation and SP1 transcriptional regulation. |
| ISSN | 00219258 |
| e-ISSN | 1083351X |
| Journal | Journal of Biological Chemistry |
| Issue Number | 31 |
| Volume Number | 290 |
| Language | English |
| Publisher | American Society for Biochemistry and Molecular Biology (United States) |
| Publisher Date | 2015-07-31 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Breast Neoplasms Genetics DNA Methylation Forkhead Transcription Factors Metabolism Neoplasms, Basal Cell Sp1 Transcription Factor Physiology Mortality Cell Movement Cell Proliferation CpG Islands Disease-Free Survival Epigenesis, Genetic Gene Expression Regulation, Neoplastic Kaplan-Meier Estimate MCF-7 Cells Molecular Sequence Data Promoter Regions, Genetic Up-Regulation Research Support, Non-U.S. Gov't Biochemistry Molecular Biology |
| Content Type | Text |
| Resource Type | Article |
| Subject | Cell Biology Biochemistry Molecular Biology |
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