Linked Life Data

10640422

Source:http://linkedlifedata.com/resource/pubmed/id/10640422

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2000-4-5
pubmed:abstractText
Growth of human breast adenocarcinoma MCF-7 cells as a tumor on nude mice is dependent on estrogen. It has been shown that estrogen withdrawal (EW) induces a partial regression of the tumor via an inhibition of cell proliferation and an induction of apoptosis. We investigated in this in vivo model the underlying molecular mechanisms of the hormone-dependent regulation of cell cycle machinery and apoptosis. We found that, 2 days after EW, the tumor protein levels of p21 rose, whereas those of Rb proteins decreased in parallel with the decrease in the proportion of tumor cells in S phase and the increase of the tumor apoptotic index. Between 3 and 7 days after EW, apoptosis was inhibited and tumor proliferation returned to the control value. There was a concomitant decline in p21 and an elevation of Rb tumor protein content. Slight variations of cyclin D protein level were observed in MCF-7 tumors over the time course following EW treatment. Bcl-2 overexpression not only inhibited apoptosis induced by EW but also modulated hormone-dependent cell cycle regulation. First, the analysis of phosphorylation status of Rb protein and the measurement of the proportion of tumor cells in S phase indicated that Bcl-2 overexpression results in a decrease of DNA synthesis induced by estradiol. Furthermore, after EW, Bcl-2-induced inhibition of hormone-dependent apoptosis was associated with an inhibition of Rb protein downregulation, a sustained level of p21 protein, and a prolonged inhibition of cell cycle progression. These results suggest that, in human hormone-dependent breast cancers, cross-talk exists between the signaling pathways which lead to regulation of cell cycle progression and apoptosis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0014-4827
pubmed:author
pubmed:copyrightInfo
Copyright 2000 Academic Press.
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
254
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
241-8
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:10640422-Animals, pubmed-meshheading:10640422-Apoptosis, pubmed-meshheading:10640422-Breast Neoplasms, pubmed-meshheading:10640422-Cell Cycle, pubmed-meshheading:10640422-Cell Cycle Proteins, pubmed-meshheading:10640422-Estradiol, pubmed-meshheading:10640422-Female, pubmed-meshheading:10640422-Genes, Retinoblastoma, pubmed-meshheading:10640422-Genes, bcl-2, pubmed-meshheading:10640422-Humans, pubmed-meshheading:10640422-In Situ Nick-End Labeling, pubmed-meshheading:10640422-Mice, pubmed-meshheading:10640422-Mice, Nude, pubmed-meshheading:10640422-Proto-Oncogene Proteins c-bcl-2, pubmed-meshheading:10640422-Receptors, Estrogen, pubmed-meshheading:10640422-Recombinant Proteins, pubmed-meshheading:10640422-Retinoblastoma Protein, pubmed-meshheading:10640422-Transfection, pubmed-meshheading:10640422-Transplantation, Heterologous, pubmed-meshheading:10640422-Tumor Cells, Cultured
pubmed:year
2000
pubmed:articleTitle
Interconnections between E2-dependent regulation of cell cycle progression and apoptosis in MCF-7 tumors growing on nude mice.
pubmed:affiliation
Laboratoire de Biologie Cellulaire et Moléculaire Contrôle de la Prolifération, CNRS, Toulouse, France. truchet@cict.fr
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't