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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1993-11-19
pubmed:abstractText
Retinoic acid (RA) has profound effects on cell proliferation and differentiation both in vitro and in vivo. Many human cell lines are known to be sensitive to the growth-inhibitory action of RA. We analyzed established human solid tumor-derived cell lines for their RA sensitivity. Growth inhibition by RA in monolayer was examined by [3H]thymidine incorporation and cell proliferation. Here we report that 11 widely used human cell lines were RA resistant. The majority are carcinoma derived (A-431, BT-20, C-41, ACHN, HCT116, 293, A549, and PA-1); two are sarcoma derived (Saos-2 and A673); and one is a melanoma cell line (A-375). Since nuclear retinoid receptors are implicated in the biological effects of RA, we examined the expression of retinoic acid receptors (RARs) RAR alpha, RAR beta, RAR gamma, and the retinoid X receptors (RXRs) RXR alpha, RXR beta, and RXR gamma in the RA-resistant cell lines by northern blotting and by RNase protection analysis for RAR beta. RAR alpha transcripts were constitutively expressed in all cell lines. By contrast, RAR beta was expressed in only seven RA-resistant cell lines (Saos-2, ACHN, 293, A549, A-375, A673, and PA-1), and its level was enhanced by RA in some cases. In most cell lines, RAR gamma expression was low and was not affected by RA. The RXR genes showed a very distinct expression pattern in the group of selected cell lines. In general, RXR alpha was the most abundantly expressed subtype, RXR beta was expressed at low levels, and RXR gamma could not be detected. In none of the RA-resistant cell lines was RXR expression modulated by RA. The results presented here indicate that the resistance of these human tumor cell lines to RA cannot be simply correlated with expression of RAR or RXR or both.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0899-1987
pubmed:author
pubmed:issnType
Print
pubmed:volume
8
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
112-22
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:7691069-Blotting, Northern, pubmed-meshheading:7691069-Cell Division, pubmed-meshheading:7691069-Cell Transformation, Neoplastic, pubmed-meshheading:7691069-Cloning, Molecular, pubmed-meshheading:7691069-Dose-Response Relationship, Drug, pubmed-meshheading:7691069-Drug Resistance, pubmed-meshheading:7691069-Gene Expression Regulation, Neoplastic, pubmed-meshheading:7691069-Humans, pubmed-meshheading:7691069-Neoplasms, pubmed-meshheading:7691069-Nuclear Proteins, pubmed-meshheading:7691069-RNA, pubmed-meshheading:7691069-Receptors, Cytoplasmic and Nuclear, pubmed-meshheading:7691069-Receptors, Retinoic Acid, pubmed-meshheading:7691069-Retinoid X Receptors, pubmed-meshheading:7691069-Transcription, Genetic, pubmed-meshheading:7691069-Transcription Factors, pubmed-meshheading:7691069-Tretinoin, pubmed-meshheading:7691069-Tumor Cells, Cultured
pubmed:year
1993
pubmed:articleTitle
Retinoic acid receptor and retinoid X receptor expression in retinoic acid-resistant human tumor cell lines.
pubmed:affiliation
Hubrecht Laboratory, Netherlands Institute for Developmental Biology, Utrecht, The Netherlands.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't