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• W1964972623 abstract "Vitamin D anti-tumor effect is often found reduced in the late stages of cancer. To uncover vitamin D resistance mechanism, we established a vitamin D-resistant human prostate cancer LNCaP cell line, LNCaP-R, by chronic exposure of cells to 1alpha,25-dihydroxyvitamin D(3) (1,25-VD). The vitamin D receptor (VDR)-mediated transcriptional activity was reduced in LNCaP-R, whereas VDR expression level and DNA-binding capacity were similar compared to parental cells (LNCaP-P). The expressions of the key factors involved in VDR transactivity, including CYP24A1 and VDR-associated proteins are all increased in LNCaP-R cells, and yet treatment with ketoconazole, P450 enzymes inhibitor, as well as trichostatin A (TSA), a histone deacetylase inhibitor, did not sensitize LNCaP-R cells response to vitamin D, suggesting that neither a local 1,25-VD availability, nor VDR-associated proteins are responsible for the vitamin D resistance. Interestingly, nuclear factor-kappaB (NF-kappaB) signaling, which is critical for 1,25-VD/VDR activity was found reduced in LNCaP-R cells, thereby treatment with NF-kappaB activator, 12-O-tetradecanoylphorbol-13-acetate (TPA), can sensitize LNCaP-R vitamin D response. Together, we conclude that NF-kappaB signaling is critical for vitamin D sensitivity, and dysregulation of this pathway would result in vitamin D resistance and disease progression." @default.
• W1964972623 created "2016-06-24" @default.
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• W1964972623 creator A5078050353 @default.
• W1964972623 creator A5090812771 @default.
• W1964972623 date "2010-05-01" @default.
• W1964972623 modified "2023-09-25" @default.
• W1964972623 title "Down-regulation of NF-κB signals is involved in loss of 1α,25-dihydroxyvitamin D3 responsiveness" @default.
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• W1964972623 doi "https://doi.org/10.1016/j.jsbmb.2010.02.030" @default.
• W1964972623 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/20206692" @default.
• W1964972623 hasPublicationYear "2010" @default.
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