MTA1

Metastasis-associated protein MTA1 is a protein that in humans is encoded by the MTA1 gene. MTA1 is the founding member of the MTA family of genes. MTA1 is primarily localized in the nucleus but also found to be distributed in the extra-nuclear compartments. MTA1 is a component of several chromatin remodeling complexes including the nucleosome remodeling and deacetylation complex (NuRD). MTA1 regulates gene expression by functioning as a coregulator to integrate DNA-interacting factors to gene activity. MTA1 participates in physiological functions in the normal and cancer cells. MTA1 is one of the most upregulated proteins in human cancer and associates with cancer progression, aggressive phenotypes, and poor prognosis of cancer patients.

Metastasis-associated protein MTA1 is a protein that in humans is encoded by the MTA1 gene. MTA1 is the founding member of the MTA family of genes. MTA1 is primarily localized in the nucleus but also found to be distributed in the extra-nuclear compartments. MTA1 is a component of several chromatin remodeling complexes including the nucleosome remodeling and deacetylation complex (NuRD). MTA1 regulates gene expression by functioning as a coregulator to integrate DNA-interacting factors to gene activity. MTA1 participates in physiological functions in the normal and cancer cells. MTA1 is one of the most upregulated proteins in human cancer and associates with cancer progression, aggressive phenotypes, and poor prognosis of cancer patients.

Cellular functions

MTA1 modulates the expression of target genes due to its ability to act as a corepressor or coactivator. MTA1 targets and/or effector pathways regulate pathways with cellular functions in both normal and cancer cells. Physiological functions of MTA1 include: its role in the brain due to MTA1 interactions with DJ1 and endophilin-3; regulation of rhodopsin expression in the mouse eye; modifier of circadian rhythm due to MTA1 interactions with the CLOCK-BMAL1 complex and stimulation of Cry-transcription; in heart development due to MTA1-FOG2 interaction; in mammary gland development as MTA1 depletion leads to ductal hypobranching, in spermatogenesis; in immunomodulation due to differential effects on the expression of cytokines in the resting and activated macrophage; in liver regeneration following hepatic injury; differentiation of mesenchymal stem cells into osteogenic axis; and a component of DNA-damage response. In cancer cells, MTA1 and its downstream effectors regulate genes and/or pathways with roles in transformation, invasion, survival, angiogenesis, epithelial-to-mesenchymal transition, metastasis, DNA damage response, and hormone-independence of breast cancer.

Notes

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