Linked Life Data

10484044

Source:http://linkedlifedata.com/resource/pubmed/id/10484044

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
1999-9-28
pubmed:abstractText
Transforming growth factor beta-1 (TGFbeta-1) causes apoptosis of many epithelial cells, including the prostate, but other secondary effects of TGFbeta-1 may be important in carcinogenesis. In a human prostate cancer cell line (ALVA-101), we determined the effects of TGFbeta-1 and TGFbeta type I and II receptor antibody on cell proliferation and TGFbeta-1 receptor binding. TGFbeta-1 and -2 and TGFbeta type II receptor mRNA expression levels were determined by polymerase chain reaction (PCR) and Northern blot analysis. A dose-responsive suppression (0.03 to 10 ng/mL) was observed for cells treated with TGFbeta-1 from 3 to 7 days (P < .01). Untreated cells had 1.1 x 10(3) (n = 3) TGFbeta receptors per cell, with a Kd of 0.20 nmol/L (n = 3) as determined by Scatchard analysis; treatment for 3 days with TGFbeta-1 (1 ng/mL) reduced the receptor number (0.9 x 10(3)) and the Kd (0.12 nmol/L). Antibodies to TGFbeta type I and II receptor stimulated proliferation with or without added TGFbeta-1 (50% +/- 5% above control, P < .01, n = 6). TGFbeta-1 and -2 and TGFbeta type II receptor mRNA expression was observed in untreated cells. In cells treated with TGFbeta-1, TGFbeta-1 mRNA was not affected by treatment, but expression levels of the TGFbeta type II receptor and TGFbeta-2 mRNA were moderately suppressed after 72 hours of treatment. Control cells actively produced TGFbeta-1 as measured by radioimmunoassay. The active and inactive forms of TGFbeta-1 were approximately equal, but TGFbeta-2 was secreted in smaller quantities than TGFbeta-1 and the inactive form of TGFbeta-2 predominated, with very small amounts of the active form. Our results suggest that the human prostate cancer cell line ALVA-101 retains negative control of proliferation in response to TGFbeta-1. Inhibition of endogenous TGFbeta action by antibodies to its receptor enhances the growth of ALVA-101 human prostate cancer cells, suggesting that endogenous TGFbeta exerts an inhibitory control on their growth and cellular function.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0026-0495
pubmed:author
pubmed:issnType
Print
pubmed:volume
48
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1075-81
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1999
pubmed:articleTitle
Transforming growth factor beta-1 and beta-2 and type II receptor functional regulation of ALVA-101 human prostate cancer cells.
pubmed:affiliation
Department of Medicine and Pathology, University of Utah School of Medicine, Salt Lake City 84132, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.