Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1994-7-5
pubmed:abstractText
Tamoxifen has been an effective antiestrogen in suppressing breast cancer growth which is estrogen-responsive or dependent. Early studies have provided circumstantial evidence that transforming growth factor-beta (TGF-beta) may be an autocrine mediator of tamoxifen action. Therefore, it is both fundamentally important and clinically relevant to investigate the relationship between tamoxifen and TGF-beta. In this study, we demonstrated that CAMA-1 cells, which are sensitive to tamoxifen inhibition, did not respond to TGF-beta growth inhibition. The type I and II TGF-beta receptors were undetectable by the radio-ligand affinity labeling technique. Despite the presence of a normal TGF-beta type II receptor gene, the mRNA transcript of the gene was undetectable by the extremely sensitive Intron-differential RNA/PCR method. The possibility that the lack of TGF-beta receptors might be intimately linked to the absence of normal retinoblastoma (Rb) gene products, as suggested by previous studies of retinoblastoma cells, was further investigated. The lack of TGF-beta receptor expression was found due to reasons other than the absence, deletion or abnormality of the Rb gene because a normal Rb gene and its hyper- and hypo-phosphorylated protein products were detected in CAMA-1 cells. In conclusion, our results suggest that the TGF-beta system is not obligatory for antiestrogen growth inhibition of CAMA-1 cells.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0730-2312
pubmed:author
pubmed:issnType
Print
pubmed:volume
54
pubmed:geneSymbol
Rb, c-myc
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
332-42
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:8200913-Base Sequence, pubmed-meshheading:8200913-Breast Neoplasms, pubmed-meshheading:8200913-Cell Division, pubmed-meshheading:8200913-Estrogens, pubmed-meshheading:8200913-Female, pubmed-meshheading:8200913-Genes, Retinoblastoma, pubmed-meshheading:8200913-Genes, myc, pubmed-meshheading:8200913-Humans, pubmed-meshheading:8200913-Molecular Sequence Data, pubmed-meshheading:8200913-Neoplasm Proteins, pubmed-meshheading:8200913-Neoplasms, Hormone-Dependent, pubmed-meshheading:8200913-Ovarian Neoplasms, pubmed-meshheading:8200913-Receptors, Transforming Growth Factor beta, pubmed-meshheading:8200913-Retinoblastoma, pubmed-meshheading:8200913-Retinoblastoma Protein, pubmed-meshheading:8200913-Tamoxifen, pubmed-meshheading:8200913-Transforming Growth Factor beta, pubmed-meshheading:8200913-Tumor Cells, Cultured
pubmed:year
1994
pubmed:articleTitle
Absence of transforming growth factor-beta responsiveness in the tamoxifen growth-inhibited human breast cancer cell line CAMA-1.
pubmed:affiliation
Department of Obstetrics and Gynecology, University of Minnesota, Minneapolis 55455.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't