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| pubmed-article:19652553 | lifeskim:mentions | umls-concept:C1101610 | lld:lifeskim |
| pubmed-article:19652553 | lifeskim:mentions | umls-concept:C1417222 | lld:lifeskim |
| pubmed-article:19652553 | lifeskim:mentions | umls-concept:C2754661 | lld:lifeskim |
| pubmed-article:19652553 | pubmed:issue | 17 | lld:pubmed |
| pubmed-article:19652553 | pubmed:dateCreated | 2009-9-8 | lld:pubmed |
| pubmed-article:19652553 | pubmed:abstractText | The hypoxia-inducible factor (HIF) pathway is essential for cell survival under low oxygen and plays an important role in tumor cell homeostasis. We investigated the function of miR-210, the most prominent microRNA upregulated by hypoxia and a direct transcriptional target of HIFs. miR-210 expression was elevated in multiple cancer types and correlated with metastasis of breast and melanoma tumors. miR-210 overexpression in cancer cell lines bypassed hypoxia-induced cell cycle arrest and partially reversed the hypoxic gene expression signature. We identified MNT, a known MYC antagonist, as a miR-210 target. MNT mRNA contains multiple miR-210 binding sites in the 3' UTR and its knockdown phenocopied miR-210 overexpression. Furthermore, loss of MYC abolished miR-210-mediated override of hypoxia-induced cell cycle arrest. Comparison of miR-210 and MYC overexpression with MNT knockdown signatures also indicated that miR-210 triggered a "MYC-like" transcriptional response. Thus, miR-210 influences the hypoxia response in tumor cells through targeting a key transcriptional repressor of the MYC-MAX network. | lld:pubmed |
| pubmed-article:19652553 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19652553 | pubmed:language | eng | lld:pubmed |
| pubmed-article:19652553 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19652553 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:19652553 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19652553 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:19652553 | pubmed:issn | 1551-4005 | lld:pubmed |
| pubmed-article:19652553 | pubmed:author | pubmed-author:HarhJ YJY | lld:pubmed |
| pubmed-article:19652553 | pubmed:author | pubmed-author:DiazRobert... | lld:pubmed |
| pubmed-article:19652553 | pubmed:author | pubmed-author:CarletonMicha... | lld:pubmed |
| pubmed-article:19652553 | pubmed:author | pubmed-author:DaiHongyueH | lld:pubmed |
| pubmed-article:19652553 | pubmed:author | pubmed-author:LinsleyPeter... | lld:pubmed |
| pubmed-article:19652553 | pubmed:author | pubmed-author:BartzSteven... | lld:pubmed |
| pubmed-article:19652553 | pubmed:author | pubmed-author:DaiXudongX | lld:pubmed |
| pubmed-article:19652553 | pubmed:author | pubmed-author:ZhangZhanZ | lld:pubmed |
| pubmed-article:19652553 | pubmed:author | pubmed-author:ChangAaron... | lld:pubmed |
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| pubmed-article:19652553 | pubmed:author | pubmed-author:SchelterJanel... | lld:pubmed |
| pubmed-article:19652553 | pubmed:author | pubmed-author:MarszalekJose... | lld:pubmed |
| pubmed-article:19652553 | pubmed:author | pubmed-author:ClearyMichele... | lld:pubmed |
| pubmed-article:19652553 | pubmed:author | pubmed-author:ImakuraMakiM | lld:pubmed |
| pubmed-article:19652553 | pubmed:author | pubmed-author:WalshRyan MRM | lld:pubmed |
| pubmed-article:19652553 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:19652553 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:19652553 | pubmed:volume | 8 | lld:pubmed |
| pubmed-article:19652553 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:19652553 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:19652553 | pubmed:pagination | 2756-68 | lld:pubmed |
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| pubmed-article:19652553 | pubmed:year | 2009 | lld:pubmed |
| pubmed-article:19652553 | pubmed:articleTitle | MicroRNA miR-210 modulates cellular response to hypoxia through the MYC antagonist MNT. | lld:pubmed |
| pubmed-article:19652553 | pubmed:affiliation | Rosetta Inpharmatics LLC, Seattle, WA, USA. microRNA210@yahoo.com | lld:pubmed |
| pubmed-article:19652553 | pubmed:publicationType | Journal Article | lld:pubmed |
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