ArticleEndocrinology2009
1Alpha,25-dihydroxyvitamin D3 reduces c-Myc expression, inhibiting proliferation and causing G1 accumulation in C4-2 prostate cancer cells.
Article in Endocrinology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
37 citing papers in PubMed, 1 synthesis or guideline pooled it, 80 citations in OpenAlex.
- Polymorphisms within Autophagy-Related Genes as Susceptibility Biomarkers for Multiple Myeloma: A Meta-Analysis of Three Large Cohorts and Functional Characterization.International journal of molecular sciences · 2023Pooled it
- ULK4 and CDKN2A polymorphisms influence the risk of developing monoclonal gammopathy of undetermined significance.International journal of cancer · 2026Article
- Vitamin D and Hypoxia: Points of Interplay in Cancer.Cancers · 2022Review
- Cytoprotective Effect of Vitamin D on Doxorubicin-Induced Cardiac Toxicity in Triple Negative Breast Cancer.International journal of molecular sciences · 2021Article
- Genomic and epigenomic active vitamin D responses in human colonic organoids.Physiological genomics · 2021Article
- The role of vitamin D and vitamin D deficiency in orthopaedics and traumatology-a narrative overview of the literature.Annals of translational medicine · 2021Review
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- Article
- Policing Cancer: Vitamin D Arrests the Cell Cycle.International journal of molecular sciences · 2020Review
- Does vitamin D deficiency predict tumour malignancy in patients with bone tumours? Data from a multi-center cohort analysis.Journal of bone oncology · 2020Article
- Vitamin D receptor knockdown attenuates the antiproliferative, pro‑apoptotic and anti‑invasive effect of vitamin D by activating the Wnt/β‑catenin signaling pathway in papillary thyroid cancer.Molecular medicine reports · 2020Article
- Vitamin D-Induced Molecular Mechanisms to Potentiate Cancer Therapy and to Reverse Drug-Resistance in Cancer Cells.Nutrients · 2020Review
- Calcitriol Inhibits Viability and Proliferation in Human Malignant Pleural Mesothelioma Cells.Frontiers in endocrinology · 2020Article
- Circulating vitamin D level and mortality in prostate cancer patients: a dose-response meta-analysis.Endocrine connections · 2018Review
- Vitamin D receptor activation reduces VCaP xenograft tumor growth and counteracts ERG activity despite induction of TMPRSS2:ERG.Oncotarget · 2017Article
- The roles of UVB and vitamin D in reducing risk of cancer incidence and mortality: A review of the epidemiology, clinical trials, and mechanisms.Reviews in endocrine & metabolic disorders · 2017Review
- Article
- The novel protein C3orf43 accelerates hepatocyte proliferation.Cellular & molecular biology letters · 2017Article
- Commonalities in the Association between PPARG and Vitamin D Related with Obesity and Carcinogenesis.PPAR research · 2016Review
- Mechanistic Effects of Calcitriol in Cancer Biology.Nutrients · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
There is an inverse correlation between exposure to sunlight (the major source of vitamin D) and the risk for prostate cancer, the most common noncutaneous cancer and second most common cause of death from cancer in American men. The active metabolite of vitamin D, 1alpha,25-dihydroxyvitamin D(3) [1,25(OH)(2)D(3)] acting through the vitamin D receptor decreases prostate cancer cell growth and invasiveness. The precise mechanisms by which 1,25(OH)(2)D(3) inhibits growth in prostate cancer have not been fully elucidated. Treatment with 1,25(OH)(2)D(3) causes an accumulation in the G(0)/G(1) phase of the cell cycle in several prostate cancer cell lines. One potential target known to regulate the G(0)/G(1) to S phase transition is c-Myc, a transcription factor whose overexpression is associated with a number of cancers including prostate cancer. We find that 1,25(OH)(2)D(3) reduces c-Myc expression in multiple prostate epithelial cell lines, including C4-2 cells, an androgen-independent prostate cancer cell line. Reducing c-Myc expression to the levels observed after 1,25(OH)(2)D(3) treatment resulted in a comparable decrease in proliferation and G(1) accumulation demonstrating that down-regulation of c-Myc is a major component in the growth-inhibitory actions of 1,25(OH)2D(3). Treatment with 1,25(OH)(2)D(3) resulted in a 50% decrease in c-Myc mRNA but a much more extensive reduction in c-Myc protein. Treatment with 1,25(OH)(2)D(3) decreased c-Myc stability by increasing the proportion of c-Myc phosphorylated on T58, a glycogen synthase kinase-3beta site that serves as a signal for ubiquitin-mediated proteolysis. Thus, 1,25(OH)(2)D(3) reduces both c-Myc mRNA levels and c-Myc protein stability to inhibit growth of prostate cancer cells.
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What OpenQuestion holds
Registered trials
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