Corepressor metastasis‐associated protein 3 modulates epithelial‐to‐mesenchymal transition and metastasis

Worldwide, metastasis is the leading cause of more than 90% of cancer‐related deaths. Currently, no specific therapies effectively impede metastasis. Metastatic processes are controlled by complex regulatory networks and transcriptional hierarchy. Corepressor metastasis‐associated protein 3 (MTA3) h...

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Bibliographic Details
Published in:Ai zheng 2017-03, Vol.36 (1), p.1-11, Article 28
Main Authors: Du, Liang, Ning, Zhifeng, Liu, Fuxing, Zhang, Hao
Format: Article
Language:English
Subjects:
Animals
Antigens
Breast cancer
Cell adhesion & migration
Co-Repressor Proteins - physiology
Coregulator
Cytoskeleton
Enzymes
Epithelial-Mesenchymal Transition
Gene expression
Humans
Kinases
Lung cancer
Master regulator
Melanoma
Metastasis
Metastasis associated proteins
Motility
Neoplasm Metastasis - physiopathology
Neoplasm Proteins - physiology
Neoplasms - pathology
Neoplasms - physiopathology
NuRD complex
Prostate
Proteins
Review
Tumors
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Summary:Worldwide, metastasis is the leading cause of more than 90% of cancer‐related deaths. Currently, no specific therapies effectively impede metastasis. Metastatic processes are controlled by complex regulatory networks and transcriptional hierarchy. Corepressor metastasis‐associated protein 3 (MTA3) has been confirmed as a novel component of nucleosome remodeling and histone deacetylation (NuRD). Increasing evidence supports the theory that, in the recruitment of transcription factors, coregulators function as master regulators rather than passive passengers. As a master regulator, MTA3 governs the target selection for NuRD and functions as a transcriptional repressor. MTA3 dysregulation is associated with tumor progression, invasion, and metastasis in various cancers. MTA3 is also a key regulator of E‐cadherin expression and epithelial‐to‐mesenchymal transition. Elucidating the functions of MTA3 might help to find additional therapeutic approaches for targeting components of NuRD.
ISSN:2523-3548
1944-446X
1000-467X
2523-3548
1944-446X
DOI:10.1186/s40880-017-0193-8