Regulation of the calcium-sensing receptor expression by 1,25-dihydroxyvitamin D3, interleukin-6, and tumor necrosis factor alpha in colon cancer cells

•1,25 Dihydroxyvitamin D3 induces the expression of CaSR in Caco2/AQ and Coga1A cells.•TNFα is the main driver of CaSR expression in Coga1A.•In Caco2/AQ cells 1,25 dihydroxyvitamin D3 counteracts the action of TNFα and IL-6. Anti-proliferative effects of calcium in the colon are mediated, at least i...

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Published in:The Journal of steroid biochemistry and molecular biology 2014-10, Vol.144, p.228-231
Main Authors: Fetahu, Irfete S., Hummel, Doris M., Manhardt, Teresa, Aggarwal, Abhishek, Baumgartner-Parzer, Sabina, Kállay, Enikő
Format: Article
Language:English
Subjects:
1,25-dihydroxyvitamin D3
Animals
Bone Density Conservation Agents - pharmacology
Calcitriol - pharmacology
Calcium-sensing receptor
Colon cancer
Colonic Neoplasms - drug therapy
Colonic Neoplasms - genetics
Colonic Neoplasms - metabolism
Gene Expression Regulation, Neoplastic - drug effects
Humans
Inflammation
Interleukin-6
Interleukin-6 - pharmacology
Receptors, Calcium-Sensing - metabolism
Tumor necrosis factor alpha
Tumor Necrosis Factor-alpha - pharmacology
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Summary:•1,25 Dihydroxyvitamin D3 induces the expression of CaSR in Caco2/AQ and Coga1A cells.•TNFα is the main driver of CaSR expression in Coga1A.•In Caco2/AQ cells 1,25 dihydroxyvitamin D3 counteracts the action of TNFα and IL-6. Anti-proliferative effects of calcium in the colon are mediated, at least in part, via the calcium-sensing receptor (CaSR), a vitamin D target gene. The expression of CaSR decreases during colorectal tumor progression and the mechanisms regulating its expression are poorly understood. The CaSR promoter harbors vitamin D elements responsive to 1,25-dihydroxyvitamin D3 (1,25D3) and NF-κB, STAT, and SP1 binding sites accounting for responsiveness to proinflammatory cytokines. Therefore, in the current study we investigated the impact of 1,25D3, tumor necrosis factor alpha (TNFα), and interleukin (IL)-6 on CaSR expression in a differentiated (Caco2/AQ) and in a moderately differentiated (Coga1A) colon cancer cell line. 1,25D3 induced CaSR expression in both cell lines. Treatment with TNFα was accompanied by a 134-fold induction of CaSR in Coga1A (p
ISSN:0960-0760
1879-1220
DOI:10.1016/j.jsbmb.2013.10.015