ArticleInternational journal of cancer2013
Increased copy-number and not DNA hypomethylation causes overexpression of the candidate proto-oncogene CYP24A1 in colorectal cancer.
Article in International journal of cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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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.
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Who cites it
41 citing papers in PubMed, 73 citations in OpenAlex.
- Association of Vitamin D Intake,Medical sciences (Basel, Switzerland) · 2026Article
- Calcitriol Modulates Age-dependent Drug Response in Paired Patient-derived Normal and Tumor Colorectal Organoids.International journal of biological sciences · 2026Article
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- Exploring potential key genes and pathways associatedwith hepatocellular carcinoma prognosis through bioinformatics analysis, followed by experimental validation.American journal of translational research · 2024Article
- Association of DNA methylation of vitamin D metabolic pathway related genes with colorectal cancer risk.Clinical epigenetics · 2023Article
- Vitamin D metabolism in cancer: potential feasibility of vitamin D metabolism blocking therapy.Medical molecular morphology · 2023Review
- Immuno-Stimulating Activity of 1,25-Dihydroxyvitamin D in Blood Cells from Five Healthy People and in Blasts from Five Patients with Leukemias and Pre-Leukemic States.International journal of molecular sciences · 2023Article
- Vitamin D Analogs Regulate the Vitamin D System and Cell Viability in Ovarian Cancer Cells.International journal of molecular sciences · 2021Article
- Squalene epoxidase promotes colorectal cancer cell proliferation through accumulating calcitriol and activating CYP24A1-mediated MAPK signaling.Cancer communications (London, England) · 2021Article
- Emerging Therapeutic Potential of SIRT6 Modulators.Journal of medicinal chemistry · 2021Review
- Is Vitamin D Deficiency Related to Increased Cancer Risk in Patients with Type 2 Diabetes Mellitus?International journal of molecular sciences · 2021Review
- Review
- The Two-Faced Role of SIRT6 in Cancer.Cancers · 2021Review
- Policing Cancer: Vitamin D Arrests the Cell Cycle.International journal of molecular sciences · 2020Review
- Small-molecule activating SIRT6 elicits therapeutic effects and synergistically promotes anti-tumor activity of vitamin DTheranostics · 2020Article
- Switching to a Healthy Diet Prevents the Detrimental Effects of Western Diet in a Colitis-Associated Colorectal Cancer Model.Nutrients · 2019Article
- The Anti-Inflammatory Effects of Vitamin D in Tumorigenesis.International journal of molecular sciences · 2018Review
- Exploring vitamin D metabolism and function in cancer.Experimental & molecular medicine · 2018Review
- Mutant Mice With Calcium-Sensing Receptor Activation Have Hyperglycemia That Is Rectified by Calcilytic Therapy.Endocrinology · 2017Article
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
In colorectal cancer (CRC) the vitamin D catabolizing enzyme 1,25-dihydroxyvitamin D 24-hydroxylase (CYP24A1) is overexpressed with a potentially significant, positive impact on the catabolism of 1,25-dihydroxyvitamin D3 (1,25-D3 ). However, the underlying mechanism of CYP24A1 overexpression is poorly understood. In the present study, we investigated possible causes including hypomethylation of the CYP24A1 promoter, amplification of the CYP24A1 gene locus (20q13.2), and altered expression of CYP24A1-specific transcription factors. We quantified CYP24A1 gene copy-number, performed bisulfite sequencing of the CYP24A1 promoter to assess DNA methylation, and measured mRNA expression of CYP24A1, 25-hydroxyvitamin D 1α-hydroxylase (CYP27B1), vitamin D receptor (VDR) and retinoid X receptor (RXR). We found that 77 (60%) out of 127 colorectal tumors showed increased CYP24A1 gene copy-number and that more than 6 copies of CYP24A1 correlated positively with CYP24A1 mRNA expression suggestive of a causal relationship. No differences in CYP24A1 promoter methylation were found between tumor tissue and adjacent mucosa from the same patient or between tissues with high or low mRNA expression, thus excluding DNA hypomethylation as a possible cause of CYP24A1 overexpression in CRC. Furthermore, mRNA expression of several factors involved in replication licensing positively correlated with CYP24A1 mRNA expression, raising the possibility that CYP24A1 overexpression might favor increased proliferation in tumors by suppressing local 1,25-D3 levels. We conclude that high copy-number gain is a key determinant of CYP24A1 overexpression in CRC. Other postulated causes of CYP24A1 overexpression including promoter hypomethylation and enhanced VDR and/or RXR expression do not appear to be involved.
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