Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2007-3-27
pubmed:abstractText
Deletions and/or loss of heterozygosity (LOH) on chromosome 15 (15q15 and 15q21) have been found in several human tumors, including carcinomas of the colorectum, breast, lung, prostate, and bladder, suggesting the presence of potential tumor suppressor gene(s) in this particular region of chromosome 15. GCIP also called CCNDBP1, DIP1, or HHM, localized at chromosome 15q15, is a recently identified helix-loop-helix leucine zipper (HLH-ZIP) protein without a basic region like the Id family of proteins. In this study, we reported that the expression of GCIP was significantly downregulated in several different human tumors, including breast tumor, prostate tumor, and colon tumors. In human colon tumors, both mRNA and protein expression levels of GCIP were decreased significantly compared to the normal tissues. Treatment of colon cancer cells SW480 with sodium butyrate (NaB), which induces colon cancer cell differentiation, can induce the upregulation of GCIP expression, suggesting that the protein functions as a negative regulator in cell proliferation. Overexpression of GCIP in SW480 colon cancer cell line resulted in a significant inhibition on tumor cell colony formation, while silencing of GCIP expression by siRNA can promote cell colony formation. Furthermore, overexpression of GCIP inhibited the transcriptional activity of cyclin D1 promoter and the expression of cyclin D1 protein in the cell. Finally, we demonstrate that GCIP specifically interacts with one of the class III HDAC proteins, SirT6, which is important for maintaining genome stability. Together, our data suggest a possible function of GCIP in tumor suppression.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0730-2312
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
100
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1376-86
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:17131381-Animals, pubmed-meshheading:17131381-Blotting, Northern, pubmed-meshheading:17131381-Blotting, Western, pubmed-meshheading:17131381-Butyrates, pubmed-meshheading:17131381-COS Cells, pubmed-meshheading:17131381-Cell Differentiation, pubmed-meshheading:17131381-Cell Line, Tumor, pubmed-meshheading:17131381-Cell Proliferation, pubmed-meshheading:17131381-Cercopithecus aethiops, pubmed-meshheading:17131381-Colonic Neoplasms, pubmed-meshheading:17131381-Cyclin D1, pubmed-meshheading:17131381-Gene Expression Regulation, Neoplastic, pubmed-meshheading:17131381-Helix-Loop-Helix Motifs, pubmed-meshheading:17131381-Histone Deacetylases, pubmed-meshheading:17131381-Humans, pubmed-meshheading:17131381-Immunohistochemistry, pubmed-meshheading:17131381-Immunoprecipitation, pubmed-meshheading:17131381-Promoter Regions, Genetic, pubmed-meshheading:17131381-Protein Binding, pubmed-meshheading:17131381-Sirtuins, pubmed-meshheading:17131381-Transcription, Genetic, pubmed-meshheading:17131381-Transcription Factors
pubmed:year
2007
pubmed:articleTitle
GCIP/CCNDBP1, a helix-loop-helix protein, suppresses tumorigenesis.
pubmed:affiliation
Institute of Biosciences and Technology, and Department of Molecular and Cellular Medicine, Texas A and M University System Health Science Center, Houston, Texas 77030, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural