2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) suppresses spheroids attachment on endometrial epithelial cells through the down-regulation of the Wnt-signaling pathway

Tsang, Hon Ki; Cheung, Tsz Yan; Kodithuwakku, Suranga P.; Chai, Joyce; Yeung, William S.B.; Wong, Chris K C; Lee, Ckf

doi:10.1016/j.reprotox.2011.11.002

Cited by 39 publications

(20 citation statements)

References 45 publications

(54 reference statements)

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“…TCDD also was found to disrupt attachment of spheroids generated from human placental choriocarcinoma cell lines to adherent human endometrial adenocarcinoma cell lines in a culture model designed to mimic embryo implantation [130]. TCDD downregulated CTNNB1 expression in the spheroids, but WNT3A or LiCl reversed the inhibitory effects of TCDD by increasing both CTNNB1 expression and the percentage of spheroids that attached to endometrial cells (Table 1).…”

Section: Effects Of Activated Ahr On Wnt Signalingmentioning

confidence: 99%

Intersection of AHR and Wnt Signaling in Development, Health, and Disease

Schneider

Branam

Peterson

2014

IJMS

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The AHR (aryl hydrocarbon receptor) and Wnt (wingless-related MMTV integration site) signaling pathways have been conserved throughout evolution. Appropriately regulated signaling through each pathway is necessary for normal development and health, while dysregulation can lead to developmental defects and disease. Though both pathways have been vigorously studied, there is relatively little research exploring the possibility of crosstalk between these pathways. In this review, we provide a brief background on (1) the roles of both AHR and Wnt signaling in development and disease, and (2) the molecular mechanisms that characterize activation of each pathway. We also discuss the need for careful and complete experimental evaluation of each pathway and describe existing research that explores the intersection of AHR and Wnt signaling. Lastly, to illustrate in detail the intersection of AHR and Wnt signaling, we summarize our recent findings which show that 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced disruption of Wnt signaling impairs fetal prostate development.

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Section: Effects Of Activated Ahr On Wnt Signalingmentioning

confidence: 99%

Intersection of AHR and Wnt Signaling in Development, Health, and Disease

Schneider

Branam

Peterson

2014

IJMS

View full text Add to dashboard Cite

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“…The doses are well within the range of Hg and TCDD levels in exposed humans, 40–42 animals 43 and in vitro studies. 44,45 Analysis of the differentially expressed genes (RNA-Seq) in the various exposures showed that 50% of the genes (486 out of 972) in the low-dose exposure (Fig. 1A) and 10% of the genes (190 out of 1888) in the high-dose exposure (Fig.…”

Section: Resultsmentioning

confidence: 99%

Identification of a unique gene expression signature in mercury and 2,3,7,8-tetrachlorodibenzo-p-dioxin co-exposed cells

et al. 2017

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Mercury (Hg) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) are major environmental contaminants that commonly co-occur in the environment. Both Hg and TCDD are associated with a number of human diseases including cancers. While the individual toxicological effects of Hg and TCDD have been extensively investigated, studies on co-exposure are limited to a few genes and pathways. Therefore, a significant knowledge gap exists in the understanding of the deleterious effects of co-exposure to Hg and TCDD. Due to the prevalence of Hg and TCDD co-contamination in the environment and the major human health hazards they pose, it is important to obtain a fuller understanding of genome-wide effects of Hg and TCDD co-exposure. In this study, by performing a comprehensive transcriptomic analysis of human bronchial epithelial cells (BEAS-2B) exposed to Hg and TCDD individually and in combination, we have uncovered a subset of genes with altered expression only in the co-exposed cells. We also identified the additive as well as antagonistic effects of Hg and TCDD on gene expression. Moreover, we found that co-exposure impacted several biological and disease processes not affected by Hg or TCDD individually. Our studies show that the consequences of Hg and TCDD co-exposure on the transcriptional program and biological processes could be substantially different from single exposures, thus providing new insights into the co-exposure-specific pathogenic processes.

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“…The assay was performed according to the previous method 62 . The JAr cells spheroids were prepared in DMEM, F-12 medium.…”

Section: Methodsmentioning

confidence: 99%

Integrin beta8 (ITGB8) activates VAV-RAC1 signaling via FAK in the acquisition of endometrial epithelial cell receptivity for blastocyst implantation

Kumar

Soni

Maurya

et al. 2017

Sci Rep

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Integrin beta8 (ITGB8) is involved in the endometrial receptivity. The blastocyst first interacts with the luminal endometrial epithelial cells during its implantation; therefore, we have investigated the signaling of ITGB8 via FAK and VAV-RAC1 in the endometrial epithelial cells. Integrin beta8 was found elevated in epithelial cells at late-pre-receptive (day4, 1600 h) and receptive (day5, 0500 h) stages of endometrial receptivity period in the mouse. Integrins downstream molecule FAK has demonstrated an increased expression and phosphorylation (Y397) in the endometrium as well as in the isolated endometrial epithelial cells during receptive and post-receptive stages. Integrin beta8 can functionally interact with FAK, VAV and RAC1 as the levels of phosphorylated-FAK, and VAV along with the RAC-GTP form was reduced after ITGB8 knockdown in the endometrial epithelial cells and uterus. Further, VAV and RAC1 were seen poorly active in the absence of FAK activity, suggesting a crosstalk of ITGB8 and FAK for VAV and RAC1 activation in the endometrial epithelial cells. Silencing of ITGB8 expression and inhibition of FAK activity in the Ishikawa cells rendered poor attachment of JAr spheroids. In conclusion, ITGB8 activates VAV-RAC1 signaling axis via FAK to facilitate the endometrial epithelial cell receptivity for the attachment of blastocyst.

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2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) suppresses spheroids attachment on endometrial epithelial cells through the down-regulation of the Wnt-signaling pathway

Cited by 39 publications

References 45 publications

Intersection of AHR and Wnt Signaling in Development, Health, and Disease

Intersection of AHR and Wnt Signaling in Development, Health, and Disease

Identification of a unique gene expression signature in mercury and 2,3,7,8-tetrachlorodibenzo-p-dioxin co-exposed cells

Integrin beta8 (ITGB8) activates VAV-RAC1 signaling via FAK in the acquisition of endometrial epithelial cell receptivity for blastocyst implantation

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