PMID- 9774664
OWN - NLM
STAT- MEDLINE
DCOM- 19981123
LR  - 20240213
IS  - 0270-7306 (Print)
IS  - 1098-5549 (Electronic)
IS  - 0270-7306 (Linking)
VI  - 18
IP  - 11
DP  - 1998 Nov
TI  - Retinoic acid receptor gamma1 (RARgamma1) levels control RARbeta2 expression in 
      SK-N-BE2(c) neuroblastoma cells and regulate a differentiation-apoptosis switch.
PG  - 6482-92
AB  - Vitamin A and its derivatives (retinoids) have profound effects on the 
      proliferation and differentiation of many cell types and are involved in a 
      diverse array of developmental and physiological regulatory processes, including 
      those responsible for the development of the mature nervous system. Retinoid 
      signals are mediated by retinoic acid (RA) receptors (RARs) and retinoid X 
      receptors (RXRs), which show distinct spatio-temporal patterns of expression 
      during development and in adult tissues. We have used SK-N-BE2(c) neuroblastoma 
      cells to study the effects of reciprocal regulation of expression of various 
      RARs. We show that in these cells RARgamma1 acts as a repressor of RARbeta2 
      transcription in the absence of an agonist. In the presence of RA, the expression 
      of RARgamma1 is reduced and that of RARbeta2 is induced. Overexpression of 
      RARgamma1 neutralizes the effects of RA on RARbeta induction. Expression of an 
      RARgamma1-specific antisense construct leads to the constitutive expression of 
      RARbeta2. Although both overexpression of RARgamma1 and its reduction of 
      expression can result in inhibition of cell proliferation, they induce different 
      morphological changes. Reduction of RARgamma1 (and induction of RARbeta) leads to 
      increased apoptosis, whereas RARgamma1 overexpression leads to differentiation in 
      the absence of apoptosis. Thus, RARgamma1 appears to control a 
      differentiation-apoptosis switch in SK-N-BE2(c) neuroblastoma cells.
FAU - Ferrari, N
AU  - Ferrari N
AD  - Laboratorio di Biologia Molecolare, Istituto Nazionale per la Ricerca sul Cancro, 
      c/o Centro di Biotecnologie Avanzate, Genoa, Italy.
FAU - Pfahl, M
AU  - Pfahl M
FAU - Levi, G
AU  - Levi G
LA  - eng
GR  - R01 CA055681/CA/NCI NIH HHS/United States
GR  - CA 55681/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Mol Cell Biol
JT  - Molecular and cellular biology
JID - 8109087
RN  - 0 (Oligonucleotides, Antisense)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Retinoic Acid)
RN  - 0 (Repressor Proteins)
RN  - 0 (Retinoid X Receptors)
RN  - 0 (Retinoids)
RN  - 0 (Transcription Factors)
RN  - 0 (retinoic acid receptor beta)
RN  - 5688UTC01R (Tretinoin)
SB  - IM
MH  - Apoptosis/*physiology
MH  - Cell Cycle/drug effects
MH  - Cell Differentiation/*physiology
MH  - Cell Division/drug effects
MH  - Gene Expression Regulation, Neoplastic/*genetics
MH  - Humans
MH  - Immunohistochemistry
MH  - Neuroblastoma/metabolism
MH  - Oligonucleotides, Antisense/genetics
MH  - RNA, Messenger/metabolism
MH  - Receptors, Retinoic Acid/genetics/*metabolism/*physiology
MH  - Repressor Proteins/metabolism
MH  - Retinoid X Receptors
MH  - Retinoids/pharmacology
MH  - Transcription Factors/genetics
MH  - Transcription, Genetic/genetics
MH  - Transcriptional Activation/physiology
MH  - Transfection/genetics
MH  - Tretinoin/pharmacology
MH  - Tumor Cells, Cultured
MH  - Retinoic Acid Receptor gamma
PMC - PMC109234
EDAT- 1998/10/17 00:00
MHDA- 1998/10/17 00:01
PMCR- 1998/11/01
CRDT- 1998/10/17 00:00
PHST- 1998/10/17 00:00 [pubmed]
PHST- 1998/10/17 00:01 [medline]
PHST- 1998/10/17 00:00 [entrez]
PHST- 1998/11/01 00:00 [pmc-release]
AID - 0296 [pii]
AID - 10.1128/MCB.18.11.6482 [doi]
PST - ppublish
SO  - Mol Cell Biol. 1998 Nov;18(11):6482-92. doi: 10.1128/MCB.18.11.6482.