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Metastasis-associated protein 1 enhances stability of hypoxia-inducible factor-1α protein by recruiting histone deacetylase 1
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Metastasis-associated protein 1 enhances stability of hypoxia-inducible factor-1α protein by recruiting histone deacetylase 1
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Metastasis-associated protein 1 enhances stability of hypoxia-inducible factor-1α protein by recruiting histone deacetylase 1
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Journal Article
Metastasis-associated protein 1 enhances stability of hypoxia-inducible factor-1α protein by recruiting histone deacetylase 1
2006
Overview
The expression of metastasis‐associated protein 1 (MTA1) correlates well with tumor metastases; however, the associated molecular mechanism is not fully understood. Here, we explored the possibility of cross‐talk between MTA1 and hypoxia‐inducible factor‐1α (HIF‐1α), a key regulator of angiogenic factors. We observed that the expression of MTA1 was strongly induced under hypoxia in breast cancer cell lines such as MCF‐7 and MDA‐MB‐231. When MTA1 was overexpressed, the transcriptional activity and stability of HIF‐1α protein were enhanced. MTA1 and HIF‐1α are physically associated
in vivo
and they were localized completely in the nucleus when coexpressed. MTA1 induced the deacetylation of HIF‐1α by increasing the expression of histone deacetylase 1 (HDAC1). MTA1 counteracted to the action of acetyltransferase, ARD1, and it did not stabilize the HIF‐1α mutant that lacks the acetylation site, K532R. These results indicate that acetylation is the major target of MTA1/HDAC1 function. Collectively, our data provide evidence of a positive cross‐talk between HIF‐1α and MTA1, which is mediated by HDAC1 recruitment, and indicate a close connection between MTA1‐associated metastasis and HIF‐1‐induced tumor angiogenesis.
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