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Synergistic inhibition of prostate cancer cell lines by a 19-nor hexafluoride vitamin D3 analogue and anti-activator protein 1 retinoid.
- Source :
-
British journal of cancer [Br J Cancer] 1999 Jan; Vol. 79 (1), pp. 101-7. - Publication Year :
- 1999
-
Abstract
- The secosteroid hormones, all-trans- and 9-cis-retinoic acid and vitamin D3, have demonstrated significant capacity to control proliferation in vitro of many solid tumour cell lines. Cooperative synergistic effects by these two ligands have been reported, and it is, therefore, possible that greater therapeutic effects could be achieved if these compounds were administered together. The role of retinoid-dependent anti-activator protein 1 (anti-AP-1) effects in controlling cancer cell proliferation appears significant. We have utilized an anti-AP-1 retinoid [2-(4,4-dimethyl-3,4-dihydro-2H-1 benzopyran-6-yl)carbonyl-2-(4-carboxyphenyl)-1,3,-dithiane; SR11238], which does not transactivate through a retinoic acid response element (RARE), and a potent vitamin D3 analogue [1alpha,25(OH)2-16-ene-23-yne-26,27-F6-19-nor-D3, code name LH] together at low, physiologically safer doses against a panel of prostate cancer cell lines that represent progressively more transformed phenotypes. The LNCaP (least transformed) and PC-3 (intermediately transformed) cell lines were synergistically inhibited in their clonal growth by the combination of LH and SR11238, whereas SR11238 alone was essentially inactive. DU-145 cells (most transformed) were completely insensitive to these analogues. LNCaP cells, but neither PC-3 nor DU-145, underwent apoptosis in the presence of LH and SR11238. Transactivation of the human osteocalcin vitamin D response element (VDRE) by LH was not enhanced in the presence of SR11238, although the expression of E-cadherin in these cells was additively up-regulated in the presence of both compounds. These data suggest the anti-AP-1 retinoid and the vitamin D3 analogue may naturally act synergistically to control cell proliferation, a process that is interrupted during transformation, and that this combination may form the basis for treatment of some androgen-independent prostate cancer.
- Subjects :
- Apoptosis drug effects
Cadherins metabolism
Cell Division drug effects
Cholecalciferol chemistry
Cholecalciferol pharmacology
Cyclin-Dependent Kinase Inhibitor p21
Cyclins metabolism
Humans
Male
Prostatic Neoplasms metabolism
Tumor Cells, Cultured
Antineoplastic Agents pharmacology
Cholecalciferol analogs & derivatives
Prostatic Neoplasms pathology
Retinoids pharmacology
Tretinoin pharmacology
Subjects
Details
- Language :
- English
- ISSN :
- 0007-0920
- Volume :
- 79
- Issue :
- 1
- Database :
- MEDLINE
- Journal :
- British journal of cancer
- Publication Type :
- Academic Journal
- Accession number :
- 10408700
- Full Text :
- https://doi.org/10.1038/sj.bjc.6690018