PMID- 7691069
OWN - NLM
STAT- MEDLINE
DCOM- 19931119
LR  - 20191023
IS  - 0899-1987 (Print)
IS  - 0899-1987 (Linking)
VI  - 8
IP  - 2
DP  - 1993
TI  - Retinoic acid receptor and retinoid X receptor expression in retinoic 
      acid-resistant human tumor cell lines.
PG  - 112-22
AB  - 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.
FAU - van der Leede, B M
AU  - van der Leede BM
AD  - Hubrecht Laboratory, Netherlands Institute for Developmental Biology, Utrecht, 
      The Netherlands.
FAU - van den Brink, C E
AU  - van den Brink CE
FAU - van der Saag, P T
AU  - van der Saag PT
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Mol Carcinog
JT  - Molecular carcinogenesis
JID - 8811105
RN  - 0 (Nuclear Proteins)
RN  - 0 (Receptors, Cytoplasmic and Nuclear)
RN  - 0 (Receptors, Retinoic Acid)
RN  - 0 (Retinoid X Receptors)
RN  - 0 (Transcription Factors)
RN  - 5688UTC01R (Tretinoin)
RN  - 63231-63-0 (RNA)
SB  - IM
MH  - Blotting, Northern
MH  - Cell Division/drug effects
MH  - Cell Transformation, Neoplastic/drug effects
MH  - Cloning, Molecular
MH  - Dose-Response Relationship, Drug
MH  - Drug Resistance
MH  - Gene Expression Regulation, Neoplastic/drug effects
MH  - Humans
MH  - Neoplasms/*metabolism/pathology
MH  - Nuclear Proteins/*biosynthesis
MH  - RNA/biosynthesis/isolation & purification
MH  - Receptors, Cytoplasmic and Nuclear/*biosynthesis/genetics
MH  - Receptors, Retinoic Acid/*biosynthesis/genetics
MH  - Retinoid X Receptors
MH  - *Transcription Factors
MH  - Transcription, Genetic/drug effects
MH  - Tretinoin/pharmacology
MH  - Tumor Cells, Cultured
EDAT- 1993/01/01 00:00
MHDA- 1993/01/01 00:01
CRDT- 1993/01/01 00:00
PHST- 1993/01/01 00:00 [pubmed]
PHST- 1993/01/01 00:01 [medline]
PHST- 1993/01/01 00:00 [entrez]
AID - 10.1002/mc.2940080208 [doi]
PST - ppublish
SO  - Mol Carcinog. 1993;8(2):112-22. doi: 10.1002/mc.2940080208.