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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
12
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pubmed:dateCreated |
2001-1-26
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pubmed:abstractText |
The effects of retinoic acid (RA) on lung cancer cells were investigated. Both all-trans (t-RA) and 13-cis RA (c-RA) decreased specific (125)I-VIP binding to NCI-H1299 cells in a time- and concentration-dependent manner. After 20 hr, 30 microM t-RA decreased specific (125)I-VIP binding by 60%. By Scatchard analysis, the density of VIP binding sites but not the affinity was reduced by 42%. NCI-H1299 VPAC(1) receptor mRNA was reduced by 48%. VIP caused a 3-fold elevation in the NCI-H1299 cAMP, and the increase in cAMP caused by VIP was reduced by 38% if the NCI-H1299 cells were treated with t-RA. Using the MTT assay, 3 microM t-RA and 3 microM c-RA inhibited NCI-H1299 proliferation by 60 and 23% respectively. Also, transforming growth factor (TGF)-beta2 increased after treatment of NCI-H1299 cells with t-RA whereas TGF-beta 1 mRNA was unaffected and TGF-beta 3 mRNA was decreased. These results suggest that RA may inhibit lung cancer growth by down-regulating VPAC(1) receptor and TGF-beta 3 mRNA but up-regulating TGF-beta 2 mRNA.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Cyclic AMP,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Vasoactive Intestinal...,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Vasoactive Intestinal...,
http://linkedlifedata.com/resource/pubmed/chemical/TGFB2 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Transforming Growth Factor beta,
http://linkedlifedata.com/resource/pubmed/chemical/Transforming Growth Factor beta2,
http://linkedlifedata.com/resource/pubmed/chemical/Transforming Growth Factor beta3,
http://linkedlifedata.com/resource/pubmed/chemical/Tretinoin
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
0196-9781
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
21
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1831-7
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:11150643-Binding Sites,
pubmed-meshheading:11150643-Cell Division,
pubmed-meshheading:11150643-Cyclic AMP,
pubmed-meshheading:11150643-Dose-Response Relationship, Drug,
pubmed-meshheading:11150643-Down-Regulation,
pubmed-meshheading:11150643-Humans,
pubmed-meshheading:11150643-Kinetics,
pubmed-meshheading:11150643-Lung Neoplasms,
pubmed-meshheading:11150643-Protein Binding,
pubmed-meshheading:11150643-RNA, Messenger,
pubmed-meshheading:11150643-Receptors, Vasoactive Intestinal Peptide,
pubmed-meshheading:11150643-Receptors, Vasoactive Intestinal Polypeptide, Type I,
pubmed-meshheading:11150643-Time Factors,
pubmed-meshheading:11150643-Transforming Growth Factor beta,
pubmed-meshheading:11150643-Transforming Growth Factor beta2,
pubmed-meshheading:11150643-Transforming Growth Factor beta3,
pubmed-meshheading:11150643-Tretinoin,
pubmed-meshheading:11150643-Tumor Cells, Cultured,
pubmed-meshheading:11150643-Up-Regulation
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pubmed:year |
2000
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pubmed:articleTitle |
Retinoic acid down-regulates VPAC(1) receptors and TGF-beta 3 but up-regulates TGF-beta 2 in lung cancer cells.
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pubmed:affiliation |
Cell & Cancer Biology Dept., Medicine Branch, National Cancer Institute, Rockville, MD 20850, USA.
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pubmed:publicationType |
Journal Article
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