ArticleOncogene2004
Androgen signaling is required for the vitamin D-mediated growth inhibition in human prostate cancer cells.
Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 68 citations in OpenAlex.
- Androgen Signaling Represses Homeobox C9, an Inhibitor of Androgen Receptor, in Prostate Cancer Cells.International journal of molecular sciences · 2026Article
- Article
- Micronutrient Food Supplements in Patients with Gastro-Intestinal and Hepatic Cancers.International journal of molecular sciences · 2021Review
- Policing Cancer: Vitamin D Arrests the Cell Cycle.International journal of molecular sciences · 2020Review
- Vitamin DCurrent nutrition reports · 2019Review
- Gender, hyperandrogenism and vitamin D deficiency related functional and morphological alterations of rat cerebral arteries.PloS one · 2019Article
- Article
- Molecular link between vitamin D and cancer prevention.Nutrients · 2013Review
- Induction of retinol-binding protein 4 and placenta-specific 8 expression in human prostate cancer cells remaining in bone following osteolytic tumor growth inhibition by osteoprotegerin.International journal of oncology · 2013Article
- Vitamin D receptor gene variants and clinical outcomes after androgen-deprivation therapy for prostate cancer.World journal of urology · 2013Article
- Inecalcitol, an analog of 1α,25(OH)(2) D(3) , induces growth arrest of androgen-dependent prostate cancer cells.International journal of cancer · 2012Article
- Suppression of prostate cancer cell rolling and adhesion to endothelium by 1α,25-dihydroxyvitamin D3.The American journal of pathology · 2011Article
- Androgen Receptor regulation of Vitamin D receptor in response of castration-resistant prostate cancer cells to 1α-Hydroxyvitamin D5 - a calcitriol analog.Genes & cancer · 2010Article
- GADD45gamma: a new vitamin D-regulated gene that is antiproliferative in prostate cancer cells.Endocrinology · 2010Article
- Tumor progression in the LPB-Tag transgenic model of prostate cancer is altered by vitamin D receptor and serum testosterone status.The Journal of steroid biochemistry and molecular biology · 2010Article
- Chimeric molecules facilitate the degradation of androgen receptors and repress the growth of LNCaP cells.Asian journal of andrology · 2009Article
- Inhibition of apoptosis in prostate cancer cells by androgens is mediated through downregulation of c-Jun N-terminal kinase activation.Neoplasia (New York, N.Y.) · 2008Article
- Suppression of RelB-mediated manganese superoxide dismutase expression reveals a primary mechanism for radiosensitization effect of 1alpha,25-dihydroxyvitamin D(3) in prostate cancer cells.Molecular cancer therapeutics · 2007Article
- Androgen receptor signaling is required for androgen-sensitive human prostate cancer cell proliferation and survival.Cancer cell international · 2005Article
- Androgen-receptor coregulators mediate the suppressive effect of androgen signals on vitamin D receptor activity.Endocrine · 2005Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epidemiological data on prostate cancer incidence has suggested that vitamin D deficiency may be a risk factor for prostate cancer. The antiproliferative activity of 1alpha, 25-dihydroxyvitamin D3 (1,25-VD) and its analogues has been demonstrated in many prostate cancer models, yet the detailed mechanisms underlying this protective effect of vitamin D remain to be determined. Here, we demonstrate that two androgen receptor (AR)-positive prostate cancer cell lines, LNCaP and CWR22R, are more sensitive to the growth inhibitory effects of 1,25-VD compared to the AR-negative prostate cancer cell lines, PC-3 and DU 145. 1,25-VD treatment inhibited cyclin-dependent kinase 2 (cdk2) activity and induced G0/G1 arrest. Interestingly, we also found that 1,25-VD treatment induced the expression of AR, and that the onset of the G0/G1 arrest in LNCaP and CWR22R cells is correlated with the onset of increasing expression of AR. This implies that the antiproliferative actions of 1,25-VD in AR-positive prostate cancer might be mediated through AR. Furthermore, a reduction in 1,25-VD-mediated growth inhibition was observed when AR signaling was blocked by antiandrogens, AR RNA interference, or targeted disruption of AR. Taken together, our data suggest that the androgen/AR signaling plays an important role in the antiproliferative effects of 1,25-VD and restoration of androgen responsiveness by 1,25-VD might be beneficial for the treatment of hormone-refractory prostate cancer patients.
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