Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1996-10-18
pubmed:abstractText
Inhibins and activins are members of the transforming growth factor-beta (TGF-beta) superfamily. Since TGF beta has been shown to be a potent proliferation-inhibiting agent for the breast cancer cell line MCF-7, we determined whether this cell line (a) transcribes messenger RNAs coding inhibin/activin alpha-, beta A-, and beta B-subunits and activin receptors, and (b) produces inhibin and/or activin proteins. Messenger RNAs for alpha- and beta-subunits of inhibin/activin and activin receptor II in MCF-7 cells were detected and localized using the reverse transcription-polymerase chain reaction (RT-PCR) analysis and in situ hybridization, respectively. The identity of the RT-PCR products was confirmed by DNA sequencing of PCR products. Immunocytochemically, inhibin and activin were localized in these cells. Our findings that messenger RNAs encoding inhibin alpha-subunit, inhibin/activin beta A-subunit, and activin receptor II were expressed, and inhibin/activin proteins were produced by MCF-7 cells, imply that these gonadal growth factors may have paracrine/autocrine functions in human breast cancer. Further, these observations suggest that these growth factors may be involved in regulating the growth and differentiation of human breast cancer cells.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0167-6806
pubmed:author
pubmed:issnType
Print
pubmed:volume
37
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
151-60
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
Expression and localization of inhibin/activin subunits and activin receptors in MCF-7 cells, a human breast cancer cell line.
pubmed:affiliation
Department of Cell and Neurobiology, University of Southern California School of Medicine, Los Angeles 90033, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.