PMID- 7641808
OWN - NLM
STAT- MEDLINE
DCOM- 19950918
LR  - 20131121
IS  - 0014-4827 (Print)
IS  - 0014-4827 (Linking)
VI  - 219
IP  - 2
DP  - 1995 Aug
TI  - Effect of 9-cis-retinoic acid on growth and RXR expression in human breast cancer 
      cells.
PG  - 555-61
AB  - A number of studies have demonstrated the ability of retinoic acid (RA) to 
      inhibit the growth of estrogen receptor-positive (ER+) human breast cancer cell 
      lines. The precise mechanism of growth inhibition is not known. However, the 
      biological effects of RA in other model systems have been shown to be mediated 
      via the nuclear retinoic acid receptors (RARs) and the retinoid X receptors 
      (RXRs). While several laboratories have examined the expression of RARs in 
      various breast cancer cell lines, no information is available concerning the role 
      of the RXRs and 9-cis-RA, the natural ligand of RXRs, in the response of breast 
      cancer cells to RA. Using a representative panel of breast cancer cell lines, we 
      determined the effect of 9-cis-RA on growth and cell cycle stage distribution, 
      analyzed steady-state mRNA levels of RXR-alpha, -beta, and -gamma, and determined 
      the effect of all-trans-RA and 9-cis-RA on RXR expression. Our results show that: 
      (1) the growth of ER+/RA-sensitive breast cancer cells is inhibited by treatment 
      with 9-cis-RA by blocking entry into S phase; (2) both ER+/RA-sensitive and 
      ER-/RA-resistant breast cancer cell lines express RXR-alpha and RXR-beta mRNAs 
      but not RXR-gamma; however, levels of these transcripts did not correlate with 
      the RA response; and (3) levels of RXR-alpha and RXR-beta mRNA were not 
      significantly altered following treatment with either all-trans-RA or 9-cis-RA. 
      These results suggest that the mechanism responsible for the retinoid sensitivity 
      of breast cancer cells does not involve transcriptional modulation of the RXRs by 
      RA.
FAU - Zhao, Z
AU  - Zhao Z
AD  - Department of Biochemistry, Temple University School of Medicine, Philadelphia, 
      Pennsylvania 19140, USA.
FAU - Zhang, Z P
AU  - Zhang ZP
FAU - Soprano, D R
AU  - Soprano DR
FAU - Soprano, K J
AU  - Soprano KJ
LA  - eng
GR  - CA 56309/CA/NCI NIH HHS/United States
GR  - CA 64945/CA/NCI NIH HHS/United States
GR  - HD 27556/HD/NICHD 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  - Exp Cell Res
JT  - Experimental cell research
JID - 0373226
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Retinoic Acid)
RN  - 0 (Retinoid X Receptors)
RN  - 0 (Transcription Factors)
RN  - 5688UTC01R (Tretinoin)
SB  - IM
MH  - Breast Neoplasms/*metabolism/*pathology
MH  - Cell Division/drug effects
MH  - Cell Line, Transformed
MH  - Female
MH  - Humans
MH  - RNA, Messenger/analysis
MH  - Receptors, Retinoic Acid/*metabolism
MH  - Retinoid X Receptors
MH  - Transcription Factors/*metabolism
MH  - Tretinoin/metabolism/*pharmacology
MH  - Tumor Cells, Cultured
EDAT- 1995/08/01 00:00
MHDA- 1995/08/01 00:01
CRDT- 1995/08/01 00:00
PHST- 1995/08/01 00:00 [pubmed]
PHST- 1995/08/01 00:01 [medline]
PHST- 1995/08/01 00:00 [entrez]
AID - S0014-4827(85)71264-5 [pii]
AID - 10.1006/excr.1995.1264 [doi]
PST - ppublish
SO  - Exp Cell Res. 1995 Aug;219(2):555-61. doi: 10.1006/excr.1995.1264.