PMID- 7593213
OWN - NLM
STAT- MEDLINE
DCOM- 19951205
LR  - 20131121
IS  - 0021-9541 (Print)
IS  - 0021-9541 (Linking)
VI  - 165
IP  - 2
DP  - 1995 Nov
TI  - Expression and regulation of retinoid X receptors in B16 melanoma cells.
PG  - 349-57
AB  - Recently, a new subfamily of nuclear retinoid receptors that is distinct from 
      that of RARs has been identified and named Retinoid X receptors (RXRs). These 
      receptors specifically bind 9-cis-retinoic acid (9cisRA), but not 
      all-trans-retinoic acid (ATRA). We determined which RXR subtypes were expressed 
      in B16 mouse melanoma cells and then studied the effect of ATRA, 8-bromo-cyclic 
      AMP (8BrcA), and phorbol dibutyrate (PDB) on RXR mRNA levels. ATRA induces 
      differentiation in these cells while 8BrcA and PDB antagonize the RA-induced 
      differentiation of B16 melanoma cells. Northern analysis demonstrated the 
      expression of RXR alpha and RXR beta mRNA in B16 cells, but RXR gamma was not 
      detectable. Further analysis using RT-PCR also failed to detect RXR gamma in 
      these cells. Long-term RA treatment decreased the expression of RXR alpha, but 
      not RXR beta mRNAs. PDB did not alter the expression of either RXR mRNAs, 
      however, 8BrcA treatment resulted in a time dependent decrease in the amount of 
      RXR beta, but not RXR alpha mRNA. Inhibition of protein synthesis by 
      cycloheximide resulted in a large increase in RXR alpha and RXR beta mRNA levels. 
      This effect of cycloheximide was time and concentration dependent with maximal 
      stimulation of RXR alpha and RXR beta mRNAs occurring at 4 h of treatment. 
      Inhibition of transcription with actinomycin D completely abolished the 
      cycloheximide-induced increase of RXR beta. In contrast to its effect on other 
      genes, such as immediate response genes, cycloheximide treatment did not increase 
      the half-life of RXR beta mRNA. Nuclear run-on assays showed that cycloheximide 
      treatment of intact B16 melanoma cells stimulated the transcription rate of RXR 
      beta, but not RXR alpha. These results suggest the presence of an unstable 
      transcription factor that negatively regulates the expression of RXR beta in B16 
      melanoma cells. In addition, since RXR beta is the predominant isotype in B16 
      cells, 8BrcA may, at least partially, inhibit RA-induced differentiation through 
      down-regulation of this RXR.
FAU - Desai, D S
AU  - Desai DS
AD  - Department of Biochemistry and Molecular Biology, Marshall University School of 
      Medicine, Huntington, West Virginia 25755-9310, USA.
FAU - Niles, R M
AU  - Niles RM
LA  - eng
PT  - Journal Article
PL  - United States
TA  - J Cell Physiol
JT  - Journal of cellular physiology
JID - 0050222
RN  - 0 (Molecular Probes)
RN  - 0 (Nuclear Proteins)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Retinoic Acid)
RN  - 0 (Retinoid X Receptors)
RN  - 0 (Transcription Factors)
RN  - 23583-48-4 (8-Bromo Cyclic Adenosine Monophosphate)
RN  - 98600C0908 (Cycloheximide)
SB  - IM
MH  - 8-Bromo Cyclic Adenosine Monophosphate/pharmacology
MH  - Animals
MH  - Base Sequence
MH  - Cell Differentiation
MH  - Cycloheximide/pharmacology
MH  - Melanoma/*metabolism/pathology
MH  - Mice
MH  - Molecular Probes/genetics
MH  - Molecular Sequence Data
MH  - Nuclear Proteins/metabolism
MH  - RNA, Messenger/metabolism
MH  - Receptors, Retinoic Acid/genetics/*metabolism
MH  - Retinoid X Receptors
MH  - Transcription Factors/genetics/*metabolism
MH  - Transcription, Genetic/drug effects
MH  - Tumor Cells, Cultured
EDAT- 1995/11/01 00:00
MHDA- 1995/11/01 00:01
CRDT- 1995/11/01 00:00
PHST- 1995/11/01 00:00 [pubmed]
PHST- 1995/11/01 00:01 [medline]
PHST- 1995/11/01 00:00 [entrez]
AID - 10.1002/jcp.1041650216 [doi]
PST - ppublish
SO  - J Cell Physiol. 1995 Nov;165(2):349-57. doi: 10.1002/jcp.1041650216.