Linked Life Data

3285997

Source:http://linkedlifedata.com/resource/pubmed/id/3285997

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
1988-6-29
pubmed:abstractText
The CA125 tumor marker is an antigenic determinant present on a high-molecular-weight glycoprotein expressed by more than 80% of newly diagnosed nonmucinous epithelial ovarian cancers. OVCA 433 human ovarian carcinoma cells express the CA125 marker at the cell surface and release large quantities of this antigen into culture medium. Here we show that release of CA125 by OVCA 433 cells is 90 to 95% inhibited by treatment with 1 x 10(-7) M dexamethasone, as determined using a biotin-based enzyme-linked immunosorbent assay utilizing OC125 monoclonal antibodies to CA125. The relative cell surface density of CA125 is also decreased following dexamethasone treatment as determined by immunofluorescence techniques using OC125 monoclonal antibodies. Inhibition of CA125 expression is specific for glucocorticoids, such as cortisol and dexamethasone, and does not occur with estrogens, progestins, androgens, or mineralocorticoids. CA125 inhibition is also dependent on the concentration of steroid used, with half-maximal and maximal inhibition by dexamethasone occurring at about 3 x 10(-9) M and 1 x 10(-7) M, respectively. Previous work has shown that OVCA 433 cells are growth inhibited by glucocorticoids and contain 14,000 glucocorticoid receptors per cell with an affinity for dexamethasone (Kd = 6.6 x 10(-9) M) which corresponds well with the concentration required for half-maximal CA125 inhibition. This correspondence, together with the specificity of CA125 inhibition for glucocorticoids, suggests that this effect is mediated by glucocorticoid receptors and is a specific biological effect of glucocorticoids on this cell type. Our results demonstrate glucocorticoid inhibition of CA125 expression by ovarian carcinoma cells and suggest that endogenous or therapeutically administered glucocorticoids can influence CA125 production by tumors in vivo.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0008-5472
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
48
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3502-6
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1988
pubmed:articleTitle
Hormonal regulation of CA125 tumor marker expression in human ovarian carcinoma cells: inhibition by glucocorticoids.
pubmed:affiliation
Department of Obstetrics and Gynecology, Yale University School of Medicine, New Haven, Connecticut 06510.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't