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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
3
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pubmed:dateCreated |
2007-12-6
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pubmed:abstractText |
Oncogene HCCR-1 functions as a negative regulator of the p53 and contributes to tumorigenesis of various human tissues. HCCR transgenic mice developed breast cancers but it is unknown how HCCR-1 contributes to human tumorigenesis. This study identified a HCCR-1-binding protein 1 (HCCRBP-1) as an HCCR binding partner by performing yeast two hybrid screening. Their endogenous interaction was further confirmed by coimmunoprecipitation experiments. These two proteins colocalized in the mitochondria. HCCRBP-1 was overexpressed in various human tumors. In addition, HCCRBP-1 alone converted NIH/3T3 cells into tumor cells in combination with no other oncogenes. HCCRBP-1 induced tumorigenesis by markedly activating PKC activities but decreasing the pro-apoptotic PKC alpha and PKC delta isoform levels. We observed that p53 stabilization also occurred with functional impairment in HCCRBP-1-transfected 293 cells, as indicated by defective induction of p21, MDM2 and bax. Indeed, HCCRBP-1 decreased p21 promoter activity probably via p53 stabilization leading to the defective function. These results indicate that HCCRBP-1 oncogene induces p53 stabilization and thereby contributes to tumorigenesis.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
1097-0215
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pubmed:author |
pubmed-author:ChoYoung-SeokYS,
pubmed-author:HaSeon-AhSA,
pubmed-author:JeonHae MyungHM,
pubmed-author:KimHyun KeeHK,
pubmed-author:KimJin WooJW,
pubmed-author:KimSangheeS,
pubmed-author:LeeHeejeongH,
pubmed-author:LeeYong JinYJ,
pubmed-author:LeeYoun SooYS,
pubmed-author:NamkoongHongH,
pubmed-author:OhChangkyuC,
pubmed-author:ParkYong GyuYG,
pubmed-author:ShinSeung MinSM
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pubmed:copyrightInfo |
(c) 2007 Wiley-Liss, Inc.
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pubmed:issnType |
Electronic
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pubmed:day |
1
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pubmed:volume |
122
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
501-8
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pubmed:meshHeading |
pubmed-meshheading:17943721-Animals,
pubmed-meshheading:17943721-Blotting, Northern,
pubmed-meshheading:17943721-Cell Transformation, Neoplastic,
pubmed-meshheading:17943721-Female,
pubmed-meshheading:17943721-Gene Expression Regulation, Neoplastic,
pubmed-meshheading:17943721-Humans,
pubmed-meshheading:17943721-Immunoprecipitation,
pubmed-meshheading:17943721-Mice,
pubmed-meshheading:17943721-Mice, Inbred BALB C,
pubmed-meshheading:17943721-Mice, Nude,
pubmed-meshheading:17943721-Mice, Transgenic,
pubmed-meshheading:17943721-NIH 3T3 Cells,
pubmed-meshheading:17943721-Oncogene Proteins,
pubmed-meshheading:17943721-Receptors, Cell Surface,
pubmed-meshheading:17943721-Saccharomyces cerevisiae,
pubmed-meshheading:17943721-Subcellular Fractions,
pubmed-meshheading:17943721-Transfection,
pubmed-meshheading:17943721-Tumor Suppressor Protein p53,
pubmed-meshheading:17943721-Two-Hybrid System Techniques,
pubmed-meshheading:17943721-beta-Galactosidase
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pubmed:year |
2008
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pubmed:articleTitle |
HCCRBP-1 directly interacting with HCCR-1 induces tumorigenesis through P53 stabilization.
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pubmed:affiliation |
Molecular Genetic Laboratory, College of Medicine, The Catholic University of Korea, Seoul 137-040, Korea.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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