Activation function 2 mediates dioxin-induced recruitment of estrogen receptor alpha to CYP1A1 and CYP1B1

MacPherson, Laura; Lo, Raymond; Ahmed, Shaimaa; Pansoy, Andrea; Matthews, Jason

doi:10.1016/j.bbrc.2009.05.060

Cited by 12 publications

(9 citation statements)

References 24 publications

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“…Meanwhile, in the coexistence of E2 and an AhR agonist, ERα‐dependent increases in AhR activity was previously proved by the mechanism of crosstalk between AhR and ERα, in which an AhR agonist induced the recruitment of ERα to the active AhR, which was enhanced in the presence of E2, and recruited ERα increased AhR transcriptional activity . More specifically, the previous study by MacPherson et al identified that both the AF1 and AF2 domains of ERα are required for ERα‐dependent increases in AhR activity, and the AF2 domain especially contributes to dioxin‐induced recruitment of ERα to AhR to induce AhR target genes such as CYP1A1 and CYP1B1 in HuH‐7 human hepatoma cells …”

Section: Discussionmentioning

confidence: 94%

Effect of dioxin and 17β-estradiol on the expression of cytochrome P450 1A1 gene via an estrogen receptor dependent pathway in cellular and xenografted models

Hwang

Kim

et al. 2017

Environmental Toxicology

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Cytochrome P450 (CYP) 1A1 plays a major role in the metabolic activation of procarcinogens to carcinogens via aryl hydrocarbon receptor (AhR) pathway. Especially, 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin (TCDD) is known as an agonist of AhR. In estrogen responsive cancers, 17β‐estradiol (E2) may influence on AhR dependent expression of CYP1 family via the interaction between estrogen receptor (ER) and AhR. In the present study, the effect of E2/ER on the expression of AhR and CYP1A1 genes was investigated for MCF‐7 clonal variant (MCF‐7 CV) breast cancer cells expressing ER. In reverse transcription‐PCR and Western blot analysis, mRNA expression level of AhR was not altered, but its protein expression level was increased by TCDD or E2. The transcriptional and translational levels of CYP1A1 appeared to be increased by TCDD or E2. The increased expression of AhR and CYP1A1 induced by E2 was restored to the control level by the co‐treatment of ICI 182,780, indicating that E2 induced the protein expression levels of AhR and CYP1A1 like TCDD via an ER dependent pathway. In an in vivo xenograft mouse model transplanted with MCF‐7 CV cells, the protein expression levels of AhR and CYP1A1 of tumor masses were also increased by E2 or TCDD. Taken together, these results indicate that E2 may promote AhR dependent expression of CYP1A1 via ER dependent pathway in MCF‐7 CV cells expressing ER in the absence of TCDD, an agonist of AhR. The relevance of E2 and ER in CYP1A1 activation of estrogen responsive cancers may be targeted for developing more effective cancer treatments.

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Section: Discussionmentioning

confidence: 94%

Effect of dioxin and 17β-estradiol on the expression of cytochrome P450 1A1 gene via an estrogen receptor dependent pathway in cellular and xenografted models

Hwang

Kim

et al. 2017

Environmental Toxicology

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“…CYP1A1 is induced by diverse exogenous and endogenous chemicals through the aryl hydrocarbone receptor [43]. Moreover, CYP1A1 expression interacts with the aryl hydrocarbone receptor and estrogen receptor alpha expression [44]. Notably, the CYP1A1 3801T>C polymorphism can alter activity and expression of the enzyme [10], [11], further regulate the expression level of aryl hydrocarbone receptor and estrogen receptor alpha, resulting in male reproduction disorders.…”

Section: Discussionmentioning

confidence: 99%

Association between 3801T>C Polymorphism of CYP1A1 and Idiopathic Male Infertility Risk: A Systematic Review and Meta-Analysis

Luo

Yao

et al. 2014

PLoS ONE

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BackgroundEpidemiological studies have evaluated the association between 3801T>C polymorphism of CYP1A1 gene and the risk for idiopathic male infertility, but the results are inconclusive. We aimed to derive a more precise estimation of the relationship by conducting a meta-analysis of case-control studies.MethodsThis study conformed to Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. PubMed, Embase and CNKI databases were searched through November 2013 to identify relevant studies. Pooled odds ratios with 95% confidence intervals were used to assess the strength of the association between CYP1A1 3801T>C polymorphism and idiopathic male infertility risk. Q-test was performed to evaluate between-study heterogeneity and publication bias was appraised using funnel plots. Sensitivity analyses were conducted to evaluate the robustness of meta-analysis findings.ResultsSix studies involving 1,060 cases and 1,225 controls were included in this meta-analysis. Overall, significant associations between 3801T>C polymorphism and idiopathic male infertility risk were observed in allelic comparison (OR = 1.36, 95% CI: 1.01–1.83), homozygous model (OR = 2.18, 95% CI: 1.15–4.12), and recessive model (OR = 1.86, 95% CI: 1.09–3.20), with robust findings according to sensitivity analyses. However, subgroup analyses did not further identify the susceptibility to idiopathic male infertility in all comparisons. Funnel plot inspections did not reveal evidence of publication bias.ConclusionsThe current meta-analysis provides evidence of a significant association between CYP1A1 3801T>C polymorphism and idiopathic male infertility risk. Considering the limitation inherited from the eligible studies, further confirmation in large-scale and well-designed studies is needed.

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“…Altogether, the CYP1B1 gene in HepG2 cells provides a valuable experimental system for further experiments focusing on potential regulatory mechanisms affecting the relationship between transcription and epigenetic modifications. Because CYP1B1 has been observed to be inducible by dioxin in other human hepatic cancer cell lines (MacPherson et al, 2009), the mechanism of inhibition of CYP1B1 expression we describe is not universal to such cell lines.…”

Section: Discussionmentioning

confidence: 82%

Role of Epigenetic Mechanisms in Differential Regulation of the Dioxin-Inducible HumanCYP1A1andCYP1B1Genes

Beedanagari

Taylor²,

Bui³

et al. 2010

Mol Pharmacol

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The aryl hydrocarbon receptor (AhR) mediates induction of CYP1A1 and CYP1B1 by 2,3,7,8-tetrachlorodibenzo--dioxin (dioxin) via binding to xenobiotic-responsive elements (XREs) in their enhancer regions. CYP1A1 and CYPIB1 were both inducible by dioxin in human MCF-7 cells. However, only CYP1A1 was inducible in human HepG2 cells. Further experiments focused on providing an explanation for this last observation. Dioxin induced the recruitment of AHR and the transcriptional coactivators p300 and p300/cAMP response element-binding protein binding protein-associated factor (PCAF) to the CYP1B1 enhancer in HepG2 cells but failed to induce recruitment of RNA polymerase II (polII) or the TATA binding protein (TBP) and acetylations of histones 3 and 4 or methylation of histone 3 at the promoter. Because p300 was required for dioxin induction of the aforementioned histone modifications at the CYP1B1 promoter and for induction of CYP1B1 transcription (in MCF-7 cells), the recruitments of p300 and AhR, although necessary, are not sufficient for eliciting the above responses to dioxin. Cytosine residues within CpG dinucleotides at the enhancer, including those within the XREs, were partially methylated, whereas those at the promoter were fully methylated. Treatment of HepG2 cells with 5-aza-2Ј-deoxycytidine led to partial demethylation of the promoter, restored polII and TBP binding, and CYP1B1 inducibility. Thus, the deficiency of CYP1B1 induction in HepG2 cells is ascribable to cytosine methylation at the promoter, which prevents recruitment of TBP and polII. It is noteworthy that our data indicate that stable recruitment of p300 and PCAF to the CYP1B1 gene does not require their tethering to the promoter and to the enhancer.

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Activation function 2 mediates dioxin-induced recruitment of estrogen receptor alpha to CYP1A1 and CYP1B1

Cited by 12 publications

References 24 publications

Effect of dioxin and 17β-estradiol on the expression of cytochrome P450 1A1 gene via an estrogen receptor dependent pathway in cellular and xenografted models

Effect of dioxin and 17β-estradiol on the expression of cytochrome P450 1A1 gene via an estrogen receptor dependent pathway in cellular and xenografted models

Association between 3801T>C Polymorphism of CYP1A1 and Idiopathic Male Infertility Risk: A Systematic Review and Meta-Analysis

Role of Epigenetic Mechanisms in Differential Regulation of the Dioxin-Inducible HumanCYP1A1andCYP1B1Genes

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