ReviewThe Journal of steroid biochemistry and molecular biology2013
1α,25(OH)2-dihydroxyvitamin D3/VDR protects the skin from UVB-induced tumor formation by interacting with the β-catenin pathway.
Review in The Journal of steroid biochemistry and molecular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
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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
30 citing papers in PubMed, 46 citations in OpenAlex.
- Potential Value of a Combination ofPharmaceuticals (Basel, Switzerland) · 2026Article
- Similarities and Differences of Vascular Calcification in Diabetes and Chronic Kidney Disease.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024Review
- Vitamin D May Protect against Breast Cancer through the Regulation of Long Noncoding RNAs by VDR Signaling.International journal of molecular sciences · 2022Review
- Vitamin D receptor gene polymorphisms and risk of breast cancer in Iranian women.Annals of medicine and surgery (2012) · 2022Article
- Vitamin D Enhances Anticancer Properties of Cediranib, a VEGFR Inhibitor, by Modulation of VEGFR2 Expression in Melanoma Cells.Frontiers in oncology · 2021Article
- Review
- Wnt and Vitamin D at the Crossroads in Solid Cancer.Cancers · 2020Review
- Review
- Anti-inflammatory and Anti-osteoporotic Potential of Lactobacillus plantarum A41 and L. fermentum SRK414 as Probiotics.Probiotics and antimicrobial proteins · 2020Article
- Skeletal and Extraskeletal Actions of Vitamin D: Current Evidence and Outstanding Questions.Endocrine reviews · 2019Review
- Neuroendocrine Aspects of Skin Aging.International journal of molecular sciences · 2019Review
- Vitamin D and its low calcemic analogs modulate the anticancer properties of cisplatin and dacarbazine in the human melanoma A375 cell line.International journal of oncology · 2019Article
- No effects without causes: the Iron Dysregulation and Dormant Microbes hypothesis for chronic, inflammatory diseases.Biological reviews of the Cambridge Philosophical Society · 2018Review
- Depleting ovarian cancer stem cells with calcitriol.Oncotarget · 2018Article
- Role of Vitamin D in Uremic Vascular Calcification.BioMed research international · 2017Review
- Promising therapies for treatment of nonalcoholic steatohepatitis.Expert opinion on emerging drugs · 2016Review
- Vitamin D derivatives enhance cytotoxic effects of H2O2 or cisplatin on human keratinocytes.Steroids · 2016Article
- Effects of 1,25(OH)2D3 on proliferation and apoptosis of human glomerular mesangial cells.American journal of translational research · 2016Article
- Role of vitamin D receptor gene polymorphisms in pancreatic cancer: a case-control study in China.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
- Vitamin D receptor, a tumor suppressor in skin.Canadian journal of physiology and pharmacology · 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
5 authors at 2 institutions in 1 country.
Funding
Abstract
Ultra violet (UV) irradiation, in particular UVB, is the single most important carcinogen for skin tumor formation. UVB induces genetic mutations and immune suppression, which lead to abnormal cell proliferation and eventually tumor formation. Previously studies from our group and others demonstrated that both global and epidermal specific VDR knock out mice are predisposed to either chemical (DMBA)- or long-term UVB-induced skin tumor formation, paralleled by an increase in β-catenin signaling. Using primary cultured human keratinocytes, we further demonstrated that 1,25(OH)2-dihydroxyvitamin D3 (1,25(OH)2D3) suppresses cyclin D1 and Gli1 which are regulated by β-catenin/TCF signaling and have a critical role in epidermal carcinogenesis. Blockage of VDR by siRNA resulted in hyperproliferation of keratinocytes, and increased expression of cyclin D1 and Gli1. In addition, we also showed that 1,25(OH)2D3/VDR directly regulates transcriptional activity of β-catenin/TCF signaling using the -catenin reporter TopGlow. Using K14 driven tamoxifen-induced cre recombinase to delete both VDR and β-catenin in keratinocytes of mice following the first hair follicle cycle, we found that ablation of epidermal specific β-catenin cannot rescue VDR null mice from UVB-induced skin tumor formation. Further study using VDR or β-catenin single null mice is necessary to compare with the data from double null mice. This article is part of a Special Issue entitled 'Vitamin D Workshop'.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.