{"doi":"10.1158/0008-5472.c.6500541","title":"Data from Epigenetic Regulation of Vitamin D 24-Hydroxylase/<i>CYP24A1</i> in Human Prostate Cancer","abstract":"<div>Abstract<p>Calcitriol, a regulator of calcium homeostasis with antitumor properties, is degraded by the product of the <i>CYP24A1</i> gene, which is downregulated in human prostate cancer by unknown mechanisms. We found that <i>CYP24A1</i> expression is inversely correlated with promoter DNA methylation in prostate cancer cell lines. Treatment with the DNA methyltransferase inhibitor 5-aza-2′-deoxycytidine (DAC) activates <i>CYP24A1</i> expression in prostate cancer cells. <i>In vitro</i> methylation of the <i>CYP24A1</i> promoter represses its promoter activity. Furthermore, inhibition of histone deacetylases by trichostatin A (TSA) enhances the expression of <i>CYP24A1</i> in prostate cancer cells. Quantitative chromatin immunoprecipitation-PCR (ChIP-qPCR) reveals that specific histone modifications are associated with the <i>CYP24A1</i> promoter region. Treatment with TSA increases H3K9ac and H3K4me2 and simultaneously decreases H3K9me2 at the <i>CYP24A1</i> promoter. ChIP-qPCR assay reveals that treatment with DAC and TSA increases the recruitment of vitamin D receptor to the <i>CYP24A1</i> promoter. Reverse transcriptase-PCR analysis of paired human prostate samples revealed that <i>CYP24A1</i> expression is downregulated in prostate malignant lesions compared with adjacent histologically benign lesions. Bisulfite pyrosequencing shows that <i>CYP24A1</i> gene is hypermethylated in malignant lesions compared with matched benign lesions. Our findings indicate that repression of <i>CYP24A1</i> gene expression in human prostate cancer cells is mediated in part by promoter DNA methylation and repressive histone modifications. Cancer Res; 70(14); 5953–62. ©2010 AACR.</p></div>","journal":null,"year":2023,"id":404936,"datarank":0.0,"base_score":0.0,"endowment":0.0,"self_citation_contribution":0.0,"citation_network_contribution":0.0,"self_endowment_contribution":0.0,"citer_contribution":0.0,"corpus_percentile":null,"corpus_rank":null,"citation_count":0,"citer_count":0,"citers_with_citation_signal":0,"citers_with_endowment":0,"datacite_reuse_total":0,"is_dataset":false,"is_dataset_confidence":0.9511,"is_data_producer":false,"deposit_databanks":null,"is_oa":true,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":"2023-01-01","fair_score":null,"fair_percentile":null,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":259920,"name":"Adam R. Karpf","orcid":"0000-0002-0866-0666","position":1,"is_corresponding":false},{"id":749978,"name":"Kristin K. Deeb","orcid":"0000-0002-2710-5406","position":2,"is_corresponding":false},{"id":1183660,"name":"Josephia R. Muindi","orcid":null,"position":3,"is_corresponding":false},{"id":396968,"name":"Carl D. Morrison","orcid":"0000-0001-7514-3098","position":4,"is_corresponding":false},{"id":368993,"name":"Candace S. Johnson","orcid":"0000-0002-1211-4692","position":5,"is_corresponding":false},{"id":601284,"name":"Donald L. Trump","orcid":null,"position":6,"is_corresponding":false},{"id":1183295,"name":"Wei Luo","orcid":"0000-0003-1431-4134","position":0,"is_corresponding":true}],"reference_count":38,"raw_metadata":null,"created_at":"2026-07-19T01:20:49.237119Z","pmid":null,"pmcid":null,"fwci":null,"citation_percentile":null,"influential_citations":0,"oa_status":null,"license":null,"views":0,"total_file_size_bytes":0,"version_count":0,"fair_f":null,"fair_a":null,"fair_i":null,"fair_r":null,"fair_zscore":null,"fair_rationale":null,"fair_model":null,"fair_agent_version":null,"fair_fulltext_source":null,"fair_has_llm":null,"fair_computed_at":null,"clinical_trials":[],"software_tools":[],"db_accessions":[],"linked_datasets":[],"topics":[]}