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Research ArticleArticle

Regulation of Human Cytosolic Sulfotransferases 1C2 and 1C3 by Nuclear Signaling Pathways in LS180 Colorectal Adenocarcinoma Cells

Elizabeth A. Rondini, Hailin Fang, Melissa Runge-Morris and Thomas A. Kocarek
Drug Metabolism and Disposition March 2014, 42 (3) 361-368; DOI: https://doi.org/10.1124/dmd.113.055673
Elizabeth A. Rondini
Institute of Environmental Health Sciences, Wayne State University, Detroit, Michigan
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Hailin Fang
Institute of Environmental Health Sciences, Wayne State University, Detroit, Michigan
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Melissa Runge-Morris
Institute of Environmental Health Sciences, Wayne State University, Detroit, Michigan
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Thomas A. Kocarek
Institute of Environmental Health Sciences, Wayne State University, Detroit, Michigan
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Abstract

Cytosolic sulfotransferases (SULTs) catalyze the sulfate conjugation of a myriad of endogenous and xenobiotic substrates. Among the 13 human SULTs, little is known regarding regulation of the SULT1C subfamily. We evaluated the effects of a panel of transcription factor activators on levels of SULT1C mRNA (1C2 and 1C3) and protein (1C2) in LS180 colorectal adenocarcinoma cells. Treatment with 3-[3-[N-(2-chloro-3-trifluoromethylbenzyl)-(2,2-diphenylethyl)amino]propyloxy]phenylacetic acid hydrochloride [GW3965, liver X receptor (LXR) activator], 3-(2,6-dichlorophenyl)-4-(3′-carboxy-2-chlorostilben-4-yl)oxymethyl-5-isopropylisoxazole [GW4064, farnesoid X receptor (FXR)], or rifampicin [pregnane X receptor (PXR)] moderately (≤2-fold) increased both SULT1C2 and SULT1C3 mRNA levels. 1α,25-Dihydroxyvitamin D3 [1,25(OH)2D3, vitamin D receptor (VDR)] selectively upregulated SULT1C2, whereas ciprofibrate [peroxisome proliferator-activated receptor α (PPARα)], rosiglitazone (PPARγ), and 2,3,7,8-tetrachlorodibenzo-p-dioxin [aryl hydrocarbon receptor (AhR)] selectively increased SULT1C3 mRNA levels. SULT1C2 protein content was strongly increased by 1,25(OH)2D3 treatment and moderately increased by GW3965, GW4064, and rifampicin. To evaluate SULT1C2 transcriptional regulation, treatment effects were determined on reporter activity from transfected constructs containing ∼10 kb of the SULT1C2 gene. Treatment with GW3965, GW4064, or 1,25(OH)2D3 increased reporter activity ∼2-, 5-, and 5.5-fold, respectively, from a construct containing mostly intron 1 of the SULT1C2 gene. Expression of AhR, LXRα, LXRβ, PPARα, PPARγ, PXR, and VDR was confirmed in LS180 cells using quantitative reverse-transcription polymerase chain reaction; however, FXR expression was negligible, suggesting that GW4064 increased SULT1C expression through an FXR-independent mechanism. Collectively, our findings are the first to characterize the regulation of human SULT1C2 and SULT1C3 expression by several transcription factor activators. Further, we determined that responsive regions for LXR and VDR are likely contained within intron 1 of the SULT1C2 gene.

Footnotes

    • Received October 30, 2013.
    • Accepted December 11, 2013.
  • This research was supported by the National Institutes of Health National Heart, Lung, and Blood Institute [Grant R01 HL050710] (to T.A.K.) and the National Institutes of Health National Institute of Environmental Health Sciences [Grant R01 ES005823] (to M.R.-M.).

  • dx.doi.org/10.1124/dmd.113.055673.

  • ↵Embedded ImageThis article has supplemental material available at dmd.aspetjournals.org.

  • Copyright © 2014 by The American Society for Pharmacology and Experimental Therapeutics
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Drug Metabolism and Disposition: 42 (3)
Drug Metabolism and Disposition
Vol. 42, Issue 3
1 Mar 2014
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Research ArticleArticle

Regulation of SULTs 1C2 and 1C3 in LS180 Cells

Elizabeth A. Rondini, Hailin Fang, Melissa Runge-Morris and Thomas A. Kocarek
Drug Metabolism and Disposition March 1, 2014, 42 (3) 361-368; DOI: https://doi.org/10.1124/dmd.113.055673

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Research ArticleArticle

Regulation of SULTs 1C2 and 1C3 in LS180 Cells

Elizabeth A. Rondini, Hailin Fang, Melissa Runge-Morris and Thomas A. Kocarek
Drug Metabolism and Disposition March 1, 2014, 42 (3) 361-368; DOI: https://doi.org/10.1124/dmd.113.055673
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