Metastasis-associated protein 1 enhances stability of hypoxia-inducible factor-1 alpha protein by recruiting histone deacetylase 1open access
- Authors
- Yoo, Young-Gun; Kong, Gu; Lee, Mi-Ock
- Issue Date
- Mar-2006
- Publisher
- WILEY
- Keywords
- HDAC1; HIF-1 alpha; hypoxia; metastasis; MTA1
- Citation
- EMBO JOURNAL, v.25, no.6, pp.1231 - 1241
- Indexed
- SCIE
SCOPUS
- Journal Title
- EMBO JOURNAL
- Volume
- 25
- Number
- 6
- Start Page
- 1231
- End Page
- 1241
- URI
- https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/181734
- DOI
- 10.1038/sj.emboj.7601025
- ISSN
- 0261-4189
- Abstract
- 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-1 alpha (HIF-1 alpha), 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-1 alpha protein were enhanced. MTA1 and HIF-1 alpha are physically associated in vivo and they were localized completely in the nucleus when coexpressed. MTA1 induced the deacetylation of HIF-1 alpha by increasing the expression of histone deacetylase 1 (HDAC1). MTA1 counteracted to the action of acetyltransferase, ARD1, and it did not stabilize the HIF-1 alpha 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-1 alpha 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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