| pubmed-article:1311629 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:1311629 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
| pubmed-article:1311629 | lifeskim:mentions | umls-concept:C0007589 | lld:lifeskim |
| pubmed-article:1311629 | lifeskim:mentions | umls-concept:C0007102 | lld:lifeskim |
| pubmed-article:1311629 | lifeskim:mentions | umls-concept:C0334227 | lld:lifeskim |
| pubmed-article:1311629 | lifeskim:mentions | umls-concept:C0596138 | lld:lifeskim |
| pubmed-article:1311629 | lifeskim:mentions | umls-concept:C0021665 | lld:lifeskim |
| pubmed-article:1311629 | lifeskim:mentions | umls-concept:C1704735 | lld:lifeskim |
| pubmed-article:1311629 | lifeskim:mentions | umls-concept:C1511941 | lld:lifeskim |
| pubmed-article:1311629 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:1311629 | pubmed:dateCreated | 1992-4-6 | lld:pubmed |
| pubmed-article:1311629 | pubmed:abstractText | The polyanionic compound suramin triggers enterocyte-like differentiation of the human colic adenocarcinoma cell clone HT29-D4. We now demonstrate that suramin interferes with the binding of IGF-I to its receptor at the surface of HT29-D4 cells. Half-maximum inhibition of 125I-IGF-I binding was obtained in the presence of 25 micrograms/ml suramin. Moreover, the drug was able to dissociate 125I-IGF previously bound to its cell surface receptor. Affinity labeling HT29-D4 cells were cultured in the presence of 10 micrograms/ml of alpha-IR3, a monoclonal antibody directed against the binding site of IGF-I, an inhibition of cell proliferation and a stimulation of cell differentiation was observed. After 10 days of treatment with alpha-IR3, HT29-D4 cells formed a regular monolayer of enterocyte-like cells exhibiting an apical brush border and tight junctions delimiting two domains of the plasma membrane (apical and basolateral). Furthermore, we show that IGF-I significantly increased the initial rate of glucose uptake by HT29-D4 cells, while we have previously shown that suramin decreased glucose consumption. From these data we conclude that IGF-I secreted by the cells themselves, stimulates proliferation of HT29-D4 cells via an autocrine mechanism. Blockade of this stimulation by suramin or by a specific monoclonal antibody inhibits cell growth, glucose uptake and triggers the process of enterocytic differentiation. | lld:pubmed |
| pubmed-article:1311629 | pubmed:language | eng | lld:pubmed |
| pubmed-article:1311629 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1311629 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:1311629 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1311629 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1311629 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1311629 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1311629 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1311629 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:1311629 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:1311629 | pubmed:issn | 0304-3835 | lld:pubmed |
| pubmed-article:1311629 | pubmed:author | pubmed-author:VerrierBB | lld:pubmed |
| pubmed-article:1311629 | pubmed:author | pubmed-author:GerardCC | lld:pubmed |
| pubmed-article:1311629 | pubmed:author | pubmed-author:FantiniJJ | lld:pubmed |
| pubmed-article:1311629 | pubmed:author | pubmed-author:BaghdiguianSS | lld:pubmed |
| pubmed-article:1311629 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:1311629 | pubmed:day | 14 | lld:pubmed |
| pubmed-article:1311629 | pubmed:volume | 62 | lld:pubmed |
| pubmed-article:1311629 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:1311629 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:1311629 | pubmed:pagination | 23-33 | lld:pubmed |
| pubmed-article:1311629 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
| pubmed-article:1311629 | pubmed:meshHeading | pubmed-meshheading:1311629-... | lld:pubmed |
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| pubmed-article:1311629 | pubmed:meshHeading | pubmed-meshheading:1311629-... | lld:pubmed |
| pubmed-article:1311629 | pubmed:meshHeading | pubmed-meshheading:1311629-... | lld:pubmed |
| pubmed-article:1311629 | pubmed:meshHeading | pubmed-meshheading:1311629-... | lld:pubmed |
| pubmed-article:1311629 | pubmed:meshHeading | pubmed-meshheading:1311629-... | lld:pubmed |
| pubmed-article:1311629 | pubmed:meshHeading | pubmed-meshheading:1311629-... | lld:pubmed |
| pubmed-article:1311629 | pubmed:year | 1992 | lld:pubmed |
| pubmed-article:1311629 | pubmed:articleTitle | Insulin like growth factor I is an autocrine regulator of human colon cancer cell differentiation and growth. | lld:pubmed |
| pubmed-article:1311629 | pubmed:affiliation | INSERM U270, Faculté de Médecine, Marseille, France. | lld:pubmed |
| pubmed-article:1311629 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:1311629 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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