Abstract | BACKGROUND: 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.
|
Authors | S de Vos, M I Dawson, S Holden, T Le, A Wang, S K Cho, D L Chen, H P Koeffler |
Journal | The Prostate
(Prostate)
Vol. 32
Issue 2
Pg. 115-21
(Jul 01 1997)
ISSN: 0270-4137 [Print] United States |
PMID | 9215399
(Publication Type: Comparative Study, Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, Non-P.H.S., Research Support, U.S. Gov't, P.H.S.)
|
Chemical References |
- Antineoplastic Agents
- Receptors, Retinoic Acid
- Retinoid X Receptors
- Retinoids
- Transcription Factor AP-1
- Transcription Factors
- Tretinoin
|
Topics |
- Antineoplastic Agents
(pharmacology)
- Cell Division
(drug effects)
- Dimerization
- Humans
- Kinetics
- Leukemia, Myeloid
- Male
- Molecular Structure
- Prostatic Neoplasms
- Receptors, Retinoic Acid
(chemistry, metabolism)
- Retinoid X Receptors
- Retinoids
(chemistry, pharmacology)
- Structure-Activity Relationship
- Transcription Factor AP-1
(antagonists & inhibitors)
- Transcription Factors
(chemistry, metabolism)
- Transcription, Genetic
- Tretinoin
(pharmacology)
- Tumor Cells, Cultured
|