Estradiol enhances and estriol inhibits the expression of CYP1A1 induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin in a mouse ovarian cancer cell line

Son, Deok‐Soo; Roby, Katherine F.; Rozman, Karl K.; Terranova, Paul F.

doi:10.1016/s0300-483x(02)00162-2

Cited by 44 publications

(29 citation statements)

References 50 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In porcine follicular cells, recent studies indicate a TCDD-induced decrease in estrogen synthesis and that the exposure to the action of AhR or ER blockers (alpha naphthoflavone and 4-OH-tamoxifen respectively) is able to completely reverse the inhibitory effect (Gregoraszczuk 2002). A further report indicates a potentiation of TCDD activity through contemporary exposure to estradiol in mouse ovarian cells, and that this effect can be reversed through exposure to specific ER blockers (Son et al 2002). Despite the fact that the precise molecular mechanisms involved in these phenomena have not been yet further investigated, these studies strongly suggest that a positive cross-talk between the two signaling pathways exists in ovarian cells.…”

Section: Ahr Cross-talk With Steroid Hormone Receptorsmentioning

confidence: 90%

Molecular interactions of the aryl hydrocarbon receptor and its biological and toxicological relevance for reproduction

Pocar

Fischer²,

Klonisch³

et al. 2005

Reproduction

167

126

View full text Add to dashboard Cite

The dioxin/aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor responsive to both natural and man-made environmental compounds. AhR and its nuclear partner ARNT are expressed in the female reproductive tract in a variety of species and several indications suggest that the AhR might play a pivotal role in the physiology of reproduction. Furthermore, it appears to be the mediator of most, if not all, the adverse effects on reproduction of a group of highly potent environmental pollutants collectively called aryl hydrocarbons (AHs), including the highly toxic compound 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Although a large body of recent literature has implicated AhR in multiple signal transduction pathways, the mechanisms of action resulting in a wide spectrum of effects on female reproduction are largely unknown. Here we summarize the major types of molecular cross-talks that have been identified for the AhR and linked cell signaling pathways and that are relevant for the understanding of the role of this transcription factor in female reproduction.

show abstract

Section: Ahr Cross-talk With Steroid Hormone Receptorsmentioning

confidence: 90%

Molecular interactions of the aryl hydrocarbon receptor and its biological and toxicological relevance for reproduction

Pocar

Fischer²,

Klonisch³

et al. 2005

Reproduction

167

126

View full text Add to dashboard Cite

show abstract

“…The effect of ERα on the AHR signaling pathway is controversial because it is influenced by cell culture conditions and exhibits cell and species specificity (35)(36)(37)(38)(47)(48)(49)(50)(51)(52). The majority of studies have focused on AHR/ERα cross talk, with few reports investigating the possible interplay between AHR and ERβ.…”

Section: Discussionmentioning

confidence: 99%

Estrogen Receptor Subtype– and Promoter-Specific Modulation of Aryl Hydrocarbon Receptor–Dependent Transcription

Wihlén

Ahmed

Inzunza

et al. 2009

Molecular Cancer Research

View full text Add to dashboard Cite

In this study, we examined the role of estrogen receptors (ER) in aryl hydrocarbon receptor (AHR)-dependent transactivation. Chromatin immunoprecipitation assays showed that AHR agonists differentially induced recruitment of ERα to the AHR target genes CYP1A1 and CYP1B1. Cotreatment with 17β-estradiol significantly increased β-naphthoflavone (BNF)-and 2,3,7,8-tetrachlorodibenzop-dioxin-induced recruitment of ERα to CYP1A1, whereas 3,3′-diindolylmethane induced promoter occupancy of ERα at CYP1A1 that was unaffected by cotreatment with 17β-estradiol. Cyclical recruitment of AHR and ERα to CYP1A1 was only observed in cells treated with BNF. Stable and subtype-specific knockdown of ERα or ERβ using shRNA showed that suppression of ERα significantly reduced, whereas knockdown of ERβ significantly enhanced, AHR agonist-induced Cyp1a1 expression in HC11 mouse mammary epithelial cells. AHR agonist-induced Cyp1b1 expression was reduced by ERβ knockdown but unaffected by ERα knockdown. The siRNA-mediated knockdown of ERα in MCF-7 human breast cancer cells did not affect 2,3,7,8-tetrachlorodibenzo-p-dioxin-dependent regulation of CYP1A1 and CYP1B1 mRNA expression. In agreement with our in vitro findings in the HC11 cells, ERα knockout mice exhibit reduced BNF-dependent induction of Cyp1a1 mRNA. These results establish ligand-and promoter-specific influences on the cyclical recruitment patterns for AHR and show ER species-, subtype-, and promoter-specific modulation of AHR-dependent transcription. (Mol Cancer Res 2009;7(6):977-86)

show abstract

“…Although a variety of genes are involved in hormone binding and metabolism, five genes in particular have been the subjects of intense investigation in hormone-related cancers: AR [15][16][17], CYP17A1 [18][19][20][21][22], CYP1A1 [23][24][25], HSD17B1, and HSD17B4 [26,27]. As testicular cancer has been hypothesized to be associated with varying levels of androgens and estrogens, genetic variants that could affect circulating levels of hormones may be important for TGCT risk.…”

Section: Introductionmentioning

confidence: 99%

Genetic variation in hormone metabolizing genes and risk of testicular germ cell tumors

Figueroa

Sakoda

Graubard

et al. 2008

Cancer Causes Control

View full text Add to dashboard Cite

Testicular germ cell tumors (TGCT) that arise in young men are composed of two histologic types, seminomas and nonseminomas. Risk patterns for the two types appear to be similar and may be related to either endogenous or exogenous hormonal exposures in utero. Why similar risk patterns would result in different histologic types is unclear, but could be related to varying genetic susceptibility profiles. Genetic variation in hormone metabolizing genes could potentially modify hormonal exposures, and thereby affect which histologic type a man develops. To examine this hypothesis, 33 single nucleotide polymorphisms (SNPs) in four hormone metabolism candidate genes (CYP1A1, CYP17A1, HSD17B1, HSD17B4) and the androgen receptor gene (AR) were genotyped. Associations with TGCT were evaluated among 577 TGCT cases (254 seminoma, 323 nonseminoma) and 707 controls from the US Servicemen's Testicular Tumor Environmental and Endocrine Determinants (STEED) study. There were no significant associations with TGCT overall based on a test using an additive model. However, compared to homozygotes of the most common allele, two nonredundant SNPs in CYP1A1 were inversely associated with nonseminoma: CYP1A1 promoter SNP rs4886605 OR = 0.75 (95% CI = 0.54-1.04) among the heterozygotes and OR = 0.37, 95% CI = 0.12-1.11 among the homozygotes with a p-value for trend = 0.02; rs2606345 intron 1 SNP, OR = 0.69 (95% CI = 0.51-0.93) among heterozygotes and OR = 0.70 (95% CI = 0.42-1.17) among homozygotes, with a p-value for trend = 0.02. Caution in interpretation is warranted until findings are replicated in other studies; however, the results suggest that genetic variation in CYP1A1 may be associated with nonseminoma.

show abstract

Estradiol enhances and estriol inhibits the expression of CYP1A1 induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin in a mouse ovarian cancer cell line

Cited by 44 publications

References 50 publications

Molecular interactions of the aryl hydrocarbon receptor and its biological and toxicological relevance for reproduction

Molecular interactions of the aryl hydrocarbon receptor and its biological and toxicological relevance for reproduction

Estrogen Receptor Subtype– and Promoter-Specific Modulation of Aryl Hydrocarbon Receptor–Dependent Transcription

Genetic variation in hormone metabolizing genes and risk of testicular germ cell tumors

Contact Info

Product

Resources

About