ArticleBritish journal of cancer2004
An antagonist of retinoic acid receptors more effectively inhibits growth of human prostate cancer cells than normal prostate epithelium.
Article in British journal of cancer, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed.
- Disruption of CDK4/6-RARα-NF-κB axis attenuates senescence-associated inflammation and improves function during aging and following chemotherapy.Nature aging · 2026Article
- Structural and Thermodynamic Discrimination between Agonists and Antagonists of Retinoic Acid Receptor γ and the Vitamin D Receptor.Journal of chemical information and modeling · 2026Article
- The Emerging Oncogenic Role of RARγ: From Stem Cell Regulation to a Potential Cancer Therapy.International journal of molecular sciences · 2025Review
- Targeting Androgen, Thyroid Hormone, and Vitamin A and D Receptors to Treat Prostate Cancer.International journal of molecular sciences · 2024Review
- Molecular Interactions of Selective Agonists and Antagonists with the Retinoic Acid Receptor γ.International journal of molecular sciences · 2024Review
- Targeting the Retinoic Acid Pathway to Eradicate Cancer Stem Cells.International journal of molecular sciences · 2023Review
- Antagonizing RARγ Drives Necroptosis of Cancer Stem Cells.International journal of molecular sciences · 2022Review
- High expression of RARG accelerates ovarian cancer progression by regulating cell proliferation.Frontiers in oncology · 2022Article
- Lessons to cancer from studies of leukemia and hematopoiesis.Frontiers in cell and developmental biology · 2022Review
- Activation of RARα Receptor Attenuates Neuroinflammation After SAHFrontiers in immunology · 2022Article
- Premature Growth Plate Closure Caused by a Hedgehog Cancer Drug Is Preventable by Co-Administration of a Retinoid Antagonist in Mice.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2021Article
- From Propargylic Alcohols to Substituted Thiochromenes:The Journal of organic chemistry · 2021Article
- The RARγ Oncogene: An Achilles Heel for Some Cancers.International journal of molecular sciences · 2021Review
- Retinoic acid receptor γ is a therapeutically targetable driver of growth and survival in prostate cancer.Cancer reports (Hoboken, N.J.) · 2020Article
- BCL-xL/MCL-1 inhibition and RARγ antagonism work cooperatively in human HL60 leukemia cells.Experimental cell research · 2014Article
- Retinoid differentiation therapy for common types of acute myeloid leukemia.Leukemia research and treatment · 2012Article
- Identification of a novel non-retinoid pan inverse agonist of the retinoic acid receptors.ACS chemical biology · 2011Article
- Oral administration of a retinoic Acid receptor antagonist reversibly inhibits spermatogenesis in mice.Endocrinology · 2011Article
- Suofu Qin's work on studies of cell survival signaling in cancer and epithelial cells.World journal of biological chemistry · 2010Article
Corrections and comments
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Screening of synthetic retinoids for activity against prostate carcinoma cell lines has identified antagonists of retinoic acid receptors (RARs) as potent growth inhibitors (Hammond et al, 2001, Br J Cancer 85, 453-462). Here we report that 5 days of exposure to a high-affinity pan-RAR antagonist (AGN194310) abolished growth of prostate carcinoma cells from 14 out of 14 patients, with half-maximal inhibition between 200 and 800 nM. It had similar effects (at approximately 250 nM) on the prostate carcinoma lines LNCaP, DU-145 and PC-3. AGN194310 inhibited the growth of normal prostate epithelium cells less potently, by 50% at approximately 1 microM. The growth of tumour cells was also inhibited more than that of normal cells when RARbeta together with RARgamma, but not RARalpha alone, were antagonised. Treatment of LNCaP cells with AGN194310 arrested them in G1 of cell cycle within 12 h, with an accompanying rise in the level of p21(waf1). The cells underwent apoptosis within 3 days, as indicated by mitochondrial depolarisation, Annexin V binding and DNA fragmentation. Apoptosis was caspase-independent: caspases were neither cleaved nor activated, and DNA fragmentation was unaffected by the pan-caspase inhibitor Z-VAD-FMK. The ability of AGN 194310 to induce apoptosis of prostate cancer cells and its differential effect on malignant and normal prostate epithelial cells suggests that this compound may be useful in the treatment of prostate cancer.
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