Polychlorinated biphenyl 104 promotes migration of endometrial stromal cells in endometriosis

Hu, Tingting; Yao, Mengyun; Fu, Xiao; Chen, Chaolu; Wu, Renyi

doi:10.1016/j.toxlet.2018.03.009

Cited by 11 publications

(14 citation statements)

References 62 publications

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“…MMP-3 contributes to the breakdown of the extracellular matrix and promotes tissue remodeling and migration [43]. The results from this study suggest that PCB-104 increased migration and invasion of ESCs through increasing MMP-3 and MMP-10 [43]. Taken together, results from tissue culture studies elucidate PCB and dioxin induced dysregulation of mechanisms potentially important in the pathophysiology of endometriosis.…”

Section: Serum and Omental Fatmentioning

confidence: 67%

“…Enzyme-linked immunosorbent assays showed a time and dose dependent increase in matrix metalloproteinase 3 (MMP-3) and MMP-10 protein in ESCs, whereas MMP-2, MMP-9, TIMP-2, E-cadherin, Snail and Slug did not. MMP-3 contributes to the breakdown of the extracellular matrix and promotes tissue remodeling and migration [43]. The results from this study suggest that PCB-104 increased migration and invasion of ESCs through increasing MMP-3 and MMP-10 [43].…”

Section: Serum and Omental Fatmentioning

confidence: 73%

“…These proteins are both critical markers for the regulation of apoptosis and cellular stress response pathways. In another study [43] primary cultures of ESCs from both case and control patients showed that PCB-104 exposure affects cell migration, invasion and resultant gene expression. Treatments induced a significant increase in cell migration and invasion of ESCs.…”

Section: Serum and Omental Fatmentioning

confidence: 98%

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The Link between Environmental Toxicant Exposure and Endometriosis Re-Examined

Freger¹,

Foster²

2021

Endometriosis

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Endometriosis is widely acknowledged to be an estrogen dependent disease or unknown etiology. Recognition that environmental toxicants can bind with and activate the estrogen receptor, dysregulate steroid metabolism and, in some cases, act as anti-androgenic substances (phthalate esters) has led to proposal that exposure to environmental toxicants are associated with increased risk of endometriosis. Since our last review of the subject in 2008, the literature has expanded with several epidemiological and biomonitoring studies suggesting a potential association, whereas others have been unable to demonstrate a link between exposure and enhanced risk. Therefore, we carried out a systematic review and critical appraisal of the literature published over the past decade (2009-2019). The majority of studies found dealt with exposure to polychlorinated biphenyls (PCBs), dioxins, dioxin-like and non-dioxin-like compounds, bisphenol A and phthalate esters. Several studies suggest a potential association between exposure to environmental toxicants; however, important weaknesses in study design, methodology, and analysis together with many contradictory studies weaken confidence in these associations. Consequently, we conclude that despite a growing literature, evidence for an association between exposure to environmental toxicants and risk of endometriosis remains weak.

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Section: Serum and Omental Fatmentioning

confidence: 67%

Section: Serum and Omental Fatmentioning

confidence: 73%

Section: Serum and Omental Fatmentioning

confidence: 98%

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The Link between Environmental Toxicant Exposure and Endometriosis Re-Examined

Freger¹,

Foster²

2021

Endometriosis

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“…It is believed that the cross-talk between EGFR and ERα plays a critical role in the regulation of breast cancer development (40). Polychlorinated biphenyl 104 was found to promote migration and invasion of endometrial stromal cells by inducing the expression of MMP-3 and MMP-10, which may involve in the EGFR signaling pathway (41). The cross talk between GPR30 and EGFR/ERK signaling pathways is supported by other studies.…”

Section: Discussionmentioning

confidence: 99%

Chronic BDE-47 Exposure Aggravates Malignant Phenotypes and Chemoresistance by Activating ERK Through ERα and GPR30 in Endometrial Carcinoma

et al. 2019

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Environmental exposure to certain compounds contribute to cell plasticity, tumor progression and even chemoresistance. 2,2′,4,4′-tetrabromo diphenyl ether (BDE-47), one of the most frequently detected polybrominated diphenyl ethers (PBDEs) in environmental and biological samples, is a known estrogen disruptor closely associated with the development of hormone-dependent cancers. However, the effect of BDE-47 on endometrial carcinoma (EC), an estrogen-dependent cancer, remains to be elucidated. Mechanisms of estrogen receptor α (ERα) and G-protein-coupled receptor-30 (GPR30) involved in BDE-47 carcinogenesis are yet to be identified. This study aims to investigate the effect of BDE-47 on the invasive phenotype of estrogen-dependent EC cells. BDE-47-treated cells, such as Ishikawa-BDE-47 and HEC-1B-BDE-47 cells, exhibited increased cell viability and enhanced metastatic ability. In vivo studies showed larger tumor volumes and more metastasis in mice injected with Ishikawa-BDE-47 cells compared with parental Ishikawa cells. MTT assay showed that BDE-47 exposure could attenuate sensitivity of EC cells to cisplatin or paclitaxel treatment in vitro. Western blotting revealed overexpression of ERα, GPR30, pEGFR (phosphorylated epidermal growth factor receptor), and pERK (phosphorylated extracellular-regulated protein kinase) in Ishikawa-BDE-47 and HEC-1B-BDE-47 cells. Knockdown of ERα or GPR30 by small interfering RNA reversed the stimulating effect of BDE-47 on cell growth, migration and invasion of EC cells. Additionally, treatment with pEGFR or pERK inhibitor impaired cell viability, migration and invasion in Ishikawa-BDE-47 and HEC-1B-BDE-47 cells. Overall, our results indicate that chronic BDE-47 exposure triggers phenotypic plasticity, promotes progression and even chemoresistance in EC cells, at least in part, via ERα/GPR30 and EGFR/ERK signaling pathways.

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“…Accumulating evidence has suggested that exposure to certain environmental endocrine chemicals, including dioxins, bisphenol A, phthalates and polychlorinated biphenyls (PCBs), may increase the risk of endometriosis (Simonelli et al 2017;Smarr et al 2016). Furthermore, our previous study has con rmed that PCBs are associated with the migration and invasion of ectopic endometrial stromal cells through in vitro culture of ectopic endometrial stromal cells (ESCs) (Hu et al 2018).…”

Section: Introductionmentioning

confidence: 89%

Prenatal polychlorinated biphenyl exposure promotes invasion of progeny ectopic endometrial stromal cells via epigenetic modification of EZH2

Wang¹,

Ye²,

Hu³

et al. 2021

Preprint

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Polychlorinated biphenyls(PCBs) are persistent environmental endocrine disruptor. This study aim to investigate the changes of the ectopic endometrium invasive ability and the possible mechanism after exposure to PCBs during pregnancy. In total, 12 female Sprague Dawley rats were intraperitoneally injected with Aroclor 1221 (1 mg/kg) or dimethyl sulfoxide (1 mg/kg) at 16 and 18 days of gestation. The endometriosis model was established by autogenous uterine abdominal wall implantation 2 months after birth. The degree of adhesion between the endometriosis and the greater omentum, as well as cell morphology and Transwell invasion patterns were used to evaluate the invasive ability of progeny ectopic endometrial stromal cells (ESCs). Moreover, the effect of the enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2)/ trimethylation of Histone 3 lysine 27 (H3K27me3) axis was examined using a highly selective EZH2 inhibitor, GSK126. After gestational PCBs exposure, the adhesion between the endometrium and the greater omentum was enhanced (P<0.05), and the length and number of microvilli were significantly increased (P<0.01). Exposure to PCBs during pregnancy increased the invasive ability of the ectopic ESCs (P<0.01), with upregulated expression levels of EZH2 and H3k27me3, which were abrogated by the EZH2 inhibitor GSK126. In conclusion, exposure to PCBs during pregnancy increased the invasive ability of the ectopic endometrium, which may be mediated by EZH2.

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Polychlorinated biphenyl 104 promotes migration of endometrial stromal cells in endometriosis

Cited by 11 publications

References 62 publications

The Link between Environmental Toxicant Exposure and Endometriosis Re-Examined

The Link between Environmental Toxicant Exposure and Endometriosis Re-Examined

Chronic BDE-47 Exposure Aggravates Malignant Phenotypes and Chemoresistance by Activating ERK Through ERα and GPR30 in Endometrial Carcinoma

Prenatal polychlorinated biphenyl exposure promotes invasion of progeny ectopic endometrial stromal cells via epigenetic modification of EZH2

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