{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Verone-Boyle AR"],"funding":["NCI NIH HHS"],"pagination":["995-1013"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4808047"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["7(1)"],"pubmed_abstract":["Epidemiologic studies implicate vitamin D status as a factor that influences growth of EGFR mutant lung cancers. However, laboratory based evidence of the biological effect of vitamin D in this disease is lacking. To fill this knowledge gap, we determined vitamin D receptor (VDR) expression in human lung tumors using a tissue microarray constructed of lung cancer cases from never-smokers (where EGFR gene mutations are prevalent). Nuclear VDR was detected in 19/19 EGFR mutant tumors. Expression tended to be higher in tumors with EGFR exon 19 deletions than those with EGFR L858R mutations. To study anti-proliferative activity and signaling, EGFR mutant lung cancer cells were treated with the circulating metabolite of vitamin D, 25-hydroxyvitamin D3 (25D3). 25D3 inhibited clonogenic growth in"],"journal":["Oncotarget"],"pubmed_title":["Diet-derived 25-hydroxyvitamin D3 activates vitamin D receptor target gene expression and suppresses EGFR mutant non-small cell lung cancer growth in vitro and in vivo."],"pmcid":["PMC4808047"],"funding_grant_id":["P30CA016056","P30 CA016056","T32CA009072","T32 CA009072","R01CA132844","R01 CA132844"],"pubmed_authors":["Verone-Boyle AR","Shoemaker S","Hershberger PA","Attwood K","Battaglia S","Makowski AJ","Morrison CD"],"additional_accession":[]},"is_claimable":false,"name":"Diet-derived 25-hydroxyvitamin D3 activates vitamin D receptor target gene expression and suppresses EGFR mutant non-small cell lung cancer growth in vitro and in vivo.","description":"Epidemiologic studies implicate vitamin D status as a factor that influences growth of EGFR mutant lung cancers. However, laboratory based evidence of the biological effect of vitamin D in this disease is lacking. To fill this knowledge gap, we determined vitamin D receptor (VDR) expression in human lung tumors using a tissue microarray constructed of lung cancer cases from never-smokers (where EGFR gene mutations are prevalent). Nuclear VDR was detected in 19/19 EGFR mutant tumors. Expression tended to be higher in tumors with EGFR exon 19 deletions than those with EGFR L858R mutations. To study anti-proliferative activity and signaling, EGFR mutant lung cancer cells were treated with the circulating metabolite of vitamin D, 25-hydroxyvitamin D3 (25D3). 25D3 inhibited clonogenic growth in","dates":{"release":"2016-01-01T00:00:00Z","publication":"2016 Jan","modification":"2025-04-19T01:27:14.153Z","creation":"2019-03-27T03:10:19Z"},"accession":"S-EPMC4808047","cross_references":{"pubmed":["26654942"],"doi":["10.18632/oncotarget.6493"]}}