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Differential gene regulation by 9-cis and all-trans retinoic acid in neuroblastoma cells.

AbstractBACKGROUND:
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.
AuthorsP E Lovat, M Dobson, A J Malcolm, A D Pearson, C P Redfern
JournalMedical and pediatric oncology (Med Pediatr Oncol) Vol. 36 Issue 1 Pg. 135-8 (Jan 2001) ISSN: 0098-1532 [Print] United States
PMID11464866 (Publication Type: Comparative Study, Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • DNA, Complementary
  • Neoplasm Proteins
  • RNA, Messenger
  • RNA, Neoplasm
  • Receptors, Retinoic Acid
  • alitretinoin
  • Tretinoin
Topics
  • 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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