Abstract | BACKGROUND: 9-cis retinoic acid (RA) is more effective than all-trans RA at inducing neuroblastoma differentiation in vitro, and has distinct biological properties with respect to its ability to promote apoptosis in N-type neuroblastoma cells. The cellular effects of 9-cis RA may, in part, result from activation of retinoid X receptor (RXR) homodimers. If this hypothesis is correct, 9-cis RA may control the expression of a different subset of retinoid-regulated genes compared to all-trans RA. PROCEDURE: We have therefore used differential mRNA display to identify genes differentially expressed in neuroblastoma cells in response to all-trans and 9-cis RA. RESULTS: The majority of cDNAs differentially expressed in response to all-trans or 9-cis RA matched to nonredundant Genbank sequences or EST database sequences. Differential-display profiles were similar in SH SY 5Y and SH S EP cells, clonal derivatives of the mixed neuroblastoma cell line SK N SH, although there were apparent differences between these cell lines with respect to the retinoid-regulation of specific RT-PCR cDNA fragments. CONCLUSIONS: These data support the view that 9-cis and all-trans RA act via different receptor mechanisms.
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Authors | P E Lovat, M Dobson, A J Malcolm, A D Pearson, C P Redfern |
Journal | Medical and pediatric oncology
(Med Pediatr Oncol)
Vol. 36
Issue 1
Pg. 135-8
(Jan 2001)
ISSN: 0098-1532 [Print] United States |
PMID | 11464866
(Publication Type: Comparative Study, Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- DNA, Complementary
- Neoplasm Proteins
- RNA, Messenger
- RNA, Neoplasm
- Receptors, Retinoic Acid
- Alitretinoin
- Tretinoin
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Topics |
- Alitretinoin
- Apoptosis
(drug effects)
- DNA, Complementary
(genetics)
- Expressed Sequence Tags
- Gene Expression Profiling
(methods)
- Gene Expression Regulation, Neoplastic
(drug effects)
- Humans
- Neoplasm Proteins
(biosynthesis, drug effects, genetics)
- RNA, Messenger
(biosynthesis)
- RNA, Neoplasm
(biosynthesis)
- Receptors, Retinoic Acid
(drug effects, physiology)
- Reverse Transcriptase Polymerase Chain Reaction
- Sequence Homology, Nucleic Acid
- Transcription, Genetic
(drug effects)
- Tretinoin
(pharmacology)
- Tumor Cells, Cultured
(drug effects)
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