Linked Life Data

15767783

Source:http://linkedlifedata.com/resource/pubmed/id/15767783

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2005-3-15
pubmed:abstractText
Deregulation of retinoblastoma gene product (pRB) is a hallmark of cancer, which acts as a transcriptional repressor by targeting E2F transcription factors. A transcription factor E2F-1 is not only important for S phase entry of cell cycle, but also stimulates gene expression of pro-apoptotic molecules. To investigate roles of E2F-1 and its target genes in cellular transformation, we studied murine E2F-1-deficient embryonic fibroblasts. Compared with control wild-type cells, E2F-1-deficient cells at early passages were less sensitive to exposure to gamma-radiation and showed an increase of colony formation, while their growth was slow. After sequential passages, the growth of E2F-1-deficient cells reached closely to that of wild-type cells. Immunoblot study of E2F target genes showed that multiple passages of E2F-1-deficient cells resulted in preferential increase of cyclin E2 expression. Furthermore, carcinogenicity study using N-nitrosomethylbenzylamine demonstrated that, compared to wild-type mice, fore-stomach tumors in E2F-1-deficient mice expressed an increased amount of cyclin E2, but not cyclin E1. Taken together, the present study shows that differential roles of E-type cyclins are involved at least partially in the process of cellular transformation, supporting the concept of important roles of the E2F regulatory pathway in carcinogenesis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1044-5498
pubmed:author
pubmed:issnType
Print
pubmed:volume
24
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
173-9
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
Differential roles of E-type cyclins during transformation of murine E2F-1-deficient cells.
pubmed:affiliation
Center for Molecular Medicine, Jichi Medical School, Tochigi, Japan. hishii@ms.jichi.ac.jp
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't