Linked Life Data

11454708

Source:http://linkedlifedata.com/resource/pubmed/id/11454708

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
14
pubmed:dateCreated
2001-7-16
pubmed:abstractText
Glypicans are a family of glycosylphosphatidylinositol-anchored cell surface heparan sulfate proteoglycans implicated in the control of cellular growth and differentiation. Here we show that glypican-1 is strongly expressed in human breast cancers, whereas expression of glypican-1 is low in normal breast tissues. In contrast, the expression of glypican-3 and -4 is only slightly increased in breast cancers by comparison with normal breast tissues, and glypican-2 and -5 are below the level of detection by Northern blotting in both normal and cancer samples. Treatment of MDA-MB-231 and MDA-MB-468 breast cancer cells with phosphoinositide-specific phospholipase-C abrogated the mitogenic response to two heparin-binding growth factors, heparin-binding epidermal growth factor-like growth factor and fibroblast growth factor 2. Stable transfection of these cells with a glypican-1 antisense construct markedly decreased glypican-1 protein levels and the mitogenic response to the same heparin-binding growth factors, as well as that to heregulin alpha, heregulin beta, and hepatocyte growth factor. Syndecan-1 was also expressed at high levels in both breast cancer tissues and breast cancer cells when compared with normal breast tissues. There was a good correlation between glypican-1 and syndecan-1 expression in the tumors. However, clones expressing the glypican-1 antisense construct did not exhibit decreased syndecan-1 levels, indicating that loss of responsiveness to heparin-binding growth factors in these clones was not due to altered syndecan-1 expression. Furthermore, 8 of 10 tumors with stage 2 or 3 disease exhibited high levels of glypican-1 by Northern blot analysis. In contrast, low levels of glypican-1 mRNA were evident in 1 of 10 tumors with stage 2 or 3 disease and in 9 of 10 tumors with stage 1 disease. Taken together, these data suggest that glypican-1 may play a pivotal role in the ability of breast cancer cells to exhibit a mitogenic response to multiple heparin-binding growth factors and may contribute to disease progression in this malignancy.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0008-5472
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
61
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
5562-9
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:11454708-Adult, pubmed-meshheading:11454708-Aged, pubmed-meshheading:11454708-Blotting, Northern, pubmed-meshheading:11454708-Breast Neoplasms, pubmed-meshheading:11454708-DNA, Antisense, pubmed-meshheading:11454708-Female, pubmed-meshheading:11454708-Gene Expression Regulation, Neoplastic, pubmed-meshheading:11454708-Growth Substances, pubmed-meshheading:11454708-Heparan Sulfate Proteoglycans, pubmed-meshheading:11454708-Humans, pubmed-meshheading:11454708-Immunohistochemistry, pubmed-meshheading:11454708-In Situ Hybridization, pubmed-meshheading:11454708-Membrane Glycoproteins, pubmed-meshheading:11454708-Middle Aged, pubmed-meshheading:11454708-Phosphatidylinositol Diacylglycerol-Lyase, pubmed-meshheading:11454708-Proteoglycans, pubmed-meshheading:11454708-RNA, Messenger, pubmed-meshheading:11454708-Syndecan-1, pubmed-meshheading:11454708-Syndecans, pubmed-meshheading:11454708-Transfection, pubmed-meshheading:11454708-Tumor Cells, Cultured, pubmed-meshheading:11454708-Type C Phospholipases
pubmed:year
2001
pubmed:articleTitle
Glypican-1 is overexpressed in human breast cancer and modulates the mitogenic effects of multiple heparin-binding growth factors in breast cancer cells.
pubmed:affiliation
Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, Biological Chemistry, and Pharmacology, University of California, Irvine, California 92697, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't