The induction of CYP1A1 by oltipraz is mediated through calcium-dependent-calpain

Dale, Yolanda; Eltom, Sakina E.

doi:10.1016/j.toxlet.2006.06.645

Cited by 4 publications

(4 citation statements)

References 26 publications

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“…Dexamethasone has been shown previously to induce Cyp1a1 at high concentrations and potentiate TCDD-induced expression in a glucocorticoid receptor and protein synthesis-dependent manner (Lai et al, 2004). Up-regulation or activation of certain transcription factors such as retinoid X receptor, PGC-1, and hepatic nuclear factor 4-␣, or calcium-dependent calpain may also contribute indirectly to Cyp1a1 induction (Gradelet et al, 1997;Dale and Eltom, 2006;Martinez-Jimenez et al, 2006). PGC-1␣ was observed to be induced by most heart and kidney treatments concurrent with Cyp1a1 up-regulation (data not shown) in which Cyp1a2, NQO1, and Ugt1a1 were not induced (Fig.…”

Section: Discussionmentioning

confidence: 91%

Induction of Cyp1a1 Is a Nonspecific Biomarker of Aryl Hydrocarbon Receptor Activation: Results of Large Scale Screening of Pharmaceuticals and Toxicants in Vivo and in Vitro

Hu¹,

et al. 2007

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Section: Discussionmentioning

confidence: 91%

Induction of Cyp1a1 Is a Nonspecific Biomarker of Aryl Hydrocarbon Receptor Activation: Results of Large Scale Screening of Pharmaceuticals and Toxicants in Vivo and in Vitro

Hu¹,

et al. 2007

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“…Furthermore, chemopreventive agent oltipraz which increases intracellular calcium, induces expression of AhR responsive gene, CYP1A1. Data presented demonstrated that oltipraz induces AhR nuclear translocation through activation of calpain [34] (Figure 4). Additional reports confirmed the enhanced elevation of intracellular calcium in response to AhR activation is associated with enhanced activity of the Ca 2+ /calmodulin (CAM)-dependent protein kinase (CaMK) pathway.…”

Section: Discussionmentioning

confidence: 99%

The Aryl Hydrocarbon Receptor: A Target for Breast Cancer Therapy

Powell¹,

Goode²,

Eltom³

2013

JCT

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The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor that regulates a battery of genes in response to exposure to a broad class of environmental poly aromatic hydrocarbons (PAH). AhR is historically characterized for its role in mediating the toxicity and adaptive responses to these chemicals, however mounting evidence has established a role for it in ligand-independent physiological processes and pathological conditions, including cancer. The AhR is overexpressed and constitutively activated in advanced breast cancer cases and was shown to drive the progression of breast cancer. In this article we will review the current state of knowledge on the possible role of AhR in breast cancer and how it will be exploited in targeting AhR for breast cancer therapy.

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“…This ligand-induced down-regulation of the receptor was shown to be blocked by inhibitors to calpain, proteasomes and nuclear export, suggesting a role for calpain and proteasome-dependent degradation and the subcellular localization (Davarinos and Pollenz 1999; Ma and Baldwin 2000; Ma, Renzelli et al 2000; Dale and Eltom 2006; Dale and Eltom 2006)a.…”

Section: Introductionmentioning

confidence: 95%

“…C. Expression of CYP1A1 mRNA in Hepa -1 WT at early (p8) and late passage (p24) following TCDD treatment for 20h (upper panel). CYP1A1 mRNA expression was determined by RT-PCR as reported previously (Dale and Eltom 2006). In lower panel, proteins isolated from trizol extract of the same treatment points used for CYP1A1 mRNA determination, were analyzed by Western blotting and probed by AhR antibody.…”

Section: Figmentioning

confidence: 99%

Stability of the aryl hydrocarbon receptor and its regulated genes in the low activity variant of Hepa-1 cell line

2015

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We examined the expression kinetics of some of the aryl hydrocarbon receptor (AhR)-regulated genes in LA1 variant cells compared to wild type (WT) Hepa-1 mouse hepatoma cell lines, and we investigated the stability of AhR protein as a key step in the function of this receptor. Treatment of both cell types with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) resulted in increased CYP1A1 and CYP1B1 mRNA with a subsequent down regulation of AhR. We show here that co-treatment with transcription inhibitor actinomycin D (ActD) has reversed the TCDD-induced depletion of AhR protein in WT. However, the proteolytic degradation of AhR in absence of TCDD was significantly higher in LA1 cells than in WT, and ActD treatment reduced this loss. Induction of CYP1A1 and CYP1B1 mRNA by TCDD in WT cells each exhibited bursts of activity in the initial hour which were about 3-fold greater than in LAI cells. The induced mRNA levels in LA1 exhibited a slow and sustained increase approximating the WT levels by 20 h. The induction of two other AhR-regulated genes also showed comparable turnover differences between the two cell types. Thus, altered regulation of the AhR responsive genes in LA1 may result from a difference in AhR stability.

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The induction of CYP1A1 by oltipraz is mediated through calcium-dependent-calpain

Cited by 4 publications

References 26 publications

Induction of Cyp1a1 Is a Nonspecific Biomarker of Aryl Hydrocarbon Receptor Activation: Results of Large Scale Screening of Pharmaceuticals and Toxicants in Vivo and in Vitro

Induction of Cyp1a1 Is a Nonspecific Biomarker of Aryl Hydrocarbon Receptor Activation: Results of Large Scale Screening of Pharmaceuticals and Toxicants in Vivo and in Vitro

The Aryl Hydrocarbon Receptor: A Target for Breast Cancer Therapy

Stability of the aryl hydrocarbon receptor and its regulated genes in the low activity variant of Hepa-1 cell line

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