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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
23
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pubmed:dateCreated |
1991-1-22
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pubmed:abstractText |
Previously, we reported that exponentially proliferating cultures of well-differentiated human colon carcinoma cells responded to transforming growth factor beta 1 (TGF-beta) with growth inhibition, alterations in morphology, and increased secretion of the differentiation marker, carcinoembryonic antigen. Poorly differentiated cultures were unresponsive. Here we show that TGF-beta was ineffective in repressing nutrient-stimulated mitogenesis in quiescent, poorly differentiated cells. However, in quiescent, well-differentiated cells, TGF-beta repressed the mitogenic responses to both nutrients alone (by 90%) and to nutrients plus the exogenous stimulatory factors epidermal growth factor (E), insulin (I), and transferrin (T) (by 55-65%). Thymidine incorporation experiments indicated that TGF-beta reduced both the onset and peak mitogenic response to growth factors and/or nutrients in the well-differentiated cells. Additionally, TGF-beta repressed the growth factor (E + I + T)-stimulated upregulation of expression of both c-myc and of transforming growth factor alpha (TGF-alpha) mRNAs in quiescent, well-differentiated cells. TGF-beta also elicited a rapid (t1/2 approximately 1h) down-regulation of c-myc expression in the absence of prior growth factor (E + I + T) stimulation. In contrast, TGF-beta had no effect on c-myc or TGF-alpha mRNA expression in the poorly differentiated cells. The results suggest that TGF-beta exerts rapid inhibitory effects on proliferation-associated genes in quiescent and restimulated, well-differentiated cells. Expression of these genes (c-myc and TGF-alpha) may otherwise (in the absence of TGF-beta) play roles in the cellular signaling of mitogenic responses by growth stimulatory factors in well-differentiated colon carcinoma cells.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Epidermal Growth Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Insulin,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-myc,
http://linkedlifedata.com/resource/pubmed/chemical/RNA,
http://linkedlifedata.com/resource/pubmed/chemical/Transferrin,
http://linkedlifedata.com/resource/pubmed/chemical/Transforming Growth Factor alpha,
http://linkedlifedata.com/resource/pubmed/chemical/Transforming Growth Factor beta
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
0008-5472
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
50
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pubmed:geneSymbol |
c-myc
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
7581-6
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:1701348-Blotting, Northern,
pubmed-meshheading:1701348-Cell Line,
pubmed-meshheading:1701348-Colonic Neoplasms,
pubmed-meshheading:1701348-Down-Regulation,
pubmed-meshheading:1701348-Epidermal Growth Factor,
pubmed-meshheading:1701348-Gene Expression Regulation, Neoplastic,
pubmed-meshheading:1701348-Humans,
pubmed-meshheading:1701348-Insulin,
pubmed-meshheading:1701348-Mitosis,
pubmed-meshheading:1701348-Proto-Oncogene Proteins c-myc,
pubmed-meshheading:1701348-RNA,
pubmed-meshheading:1701348-Transferrin,
pubmed-meshheading:1701348-Transforming Growth Factor alpha,
pubmed-meshheading:1701348-Transforming Growth Factor beta
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pubmed:year |
1990
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pubmed:articleTitle |
Inhibitory effects of transforming growth factor beta 1 on mitogenic response, transforming growth factor alpha, and c-myc in quiescent, well-differentiated colon carcinoma cells.
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pubmed:affiliation |
Department of Pharmacology, Baylor College of Medicine, Houston, Texas 77030.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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