PMID- 9215399
OWN - NLM
STAT- MEDLINE
DCOM- 19970804
LR  - 20190914
IS  - 0270-4137 (Print)
IS  - 0270-4137 (Linking)
VI  - 32
IP  - 2
DP  - 1997 Jul 1
TI  - Effects of retinoid X receptor-selective ligands on proliferation of prostate 
      cancer cells.
PG  - 115-21
AB  - BACKGROUND: Management of prostate cancer that either is detectable by prostate 
      specific antigen (PSA) measurements after curative intent or has spread outside 
      of its capsule is a serious problem. Innovative, nontoxic approaches to the 
      disease are required. One approach might be therapy with retinoids. Retinoid 
      activities are mediated by two distinct families of transcription factors: the 
      retinoic acid receptors (RARs) and retinoid X receptors (RXRs), which can induce 
      transcriptional activation through specific DNA sites or by inhibiting the 
      transcription factor AP-1 that usually mediates cellular proliferative signals. 
      The RARs require heterodimerization with RXRs. RXRs can form either heterodimers 
      or homodimers; and the latter can bind to DNA response elements that are distinct 
      from those bound by the RAR/RXR heterodimers. METHODS: A series of novel 
      synthetic retinoids that selectively interact with RXR/RXR homodimers or RAR/RXR 
      heterodimers, or that selectively inhibit AP-1 activity without activating 
      transcription were evaluated for their ability to inhibit clonal growth of three 
      human prostate cancer cell lines (PC-3, DU-145, and LNCaP). RESULTS: Several 
      notable findings were: 1) RXR-selective retinoids, such as SR11246, were able to 
      inhibit the clonal growth of prostate cancer cells. In contrast, SR11246 had 
      little effect on clonal growth of myeloid leukemic cells. 2) RAR-selective 
      retinoids also inhibited clonal growth of prostate cancer cells. 3) The retinoid 
      (SR11238) with potent anti-AP-1 activity had no effect on the clonal growth of 
      prostate cancer cells. CONCLUSIONS: This study shows that both RXR- and 
      RAR-selective retinoids are worthy of further study and may be candidates for 
      future clinical trials in prostate cancer.
FAU - de Vos, S
AU  - de Vos S
AD  - Division of Hemotology/Oncology, UCLA School of Medicine 90048, USA.
FAU - Dawson, M I
AU  - Dawson MI
FAU - Holden, S
AU  - Holden S
FAU - Le, T
AU  - Le T
FAU - Wang, A
AU  - Wang A
FAU - Cho, S K
AU  - Cho SK
FAU - Chen, D L
AU  - Chen DL
FAU - Koeffler, H P
AU  - Koeffler HP
LA  - eng
GR  - CA-26038/CA/NCI NIH HHS/United States
GR  - CA-42710/CA/NCI NIH HHS/United States
GR  - CA-43277/CA/NCI NIH HHS/United States
GR  - etc.
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Prostate
JT  - The Prostate
JID - 8101368
RN  - 0 (Antineoplastic Agents)
RN  - 0 (Receptors, Retinoic Acid)
RN  - 0 (Retinoid X Receptors)
RN  - 0 (Retinoids)
RN  - 0 (Transcription Factor AP-1)
RN  - 0 (Transcription Factors)
RN  - 5688UTC01R (Tretinoin)
SB  - IM
MH  - Antineoplastic Agents/*pharmacology
MH  - Cell Division/drug effects
MH  - Dimerization
MH  - Humans
MH  - Kinetics
MH  - Leukemia, Myeloid
MH  - Male
MH  - Molecular Structure
MH  - Prostatic Neoplasms
MH  - Receptors, Retinoic Acid/chemistry/*metabolism
MH  - Retinoid X Receptors
MH  - Retinoids/chemistry/*pharmacology
MH  - Structure-Activity Relationship
MH  - Transcription Factor AP-1/antagonists & inhibitors
MH  - Transcription Factors/chemistry/*metabolism
MH  - Transcription, Genetic
MH  - Tretinoin/pharmacology
MH  - Tumor Cells, Cultured
EDAT- 1997/07/01 00:00
MHDA- 2000/06/20 09:00
CRDT- 1997/07/01 00:00
PHST- 1997/07/01 00:00 [pubmed]
PHST- 2000/06/20 09:00 [medline]
PHST- 1997/07/01 00:00 [entrez]
AID - 10.1002/(SICI)1097-0045(19970701)32:2<115::AID-PROS6>3.0.CO;2-L [pii]
AID - 10.1002/(sici)1097-0045(19970701)32:2<115::aid-pros6>3.0.co;2-l [doi]
PST - ppublish
SO  - Prostate. 1997 Jul 1;32(2):115-21. doi: 
      10.1002/(sici)1097-0045(19970701)32:2<115::aid-pros6>3.0.co;2-l.