Bisphenol A affects estradiol metabolism by targeting CYP1A1 and CYP19A1 in human placental JEG-3 cells

Xu, Huangfang; Zhang, Xiaolei; Ye, Yunzhen; Li, Xiaotian

doi:10.1016/j.tiv.2019.104615

Cited by 30 publications

(24 citation statements)

References 45 publications

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“…In line with our results, CYN was previously shown to up-regulate CYP1A1, and other CYP isoforms (CYP1B1 and CYP1A2) in HepG2 cells [18,[25][26][27] and human peripheral blood lymphocytes (HPBLs) [26]. Recently, the up-regulation of the expression of CYP1A1 was reported following the exposure to BPs (BPA, BPS, BPF, and BPAF) in HepG2 cells [46] and the up-regulation of CYP1A1 on the protein level following exposure to BPA in human placental JEG-3 choriocarcinoma cells was reported [74].…”

Section: Dna Damage Response Genesmentioning

confidence: 98%

“…In the CYN/BPA treated cells, even synergistic action was indicated as CYP1A1 up-regulation induced by CYN/BPA (12.4-fold) was higher than the sum up-regulation induced by the single compounds (CYN 2.7-fold and BPA 5.3-fold). of CYP1A1 on the protein level following exposure to BPA in human placental JEG-3 choriocarcinoma cells was reported [74].…”

Section: Xenobiotic Metabolism-cyp1a1mentioning

confidence: 99%

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Plastics in Cyanobacterial Blooms—Genotoxic Effects of Binary Mixtures of Cylindrospermopsin and Bisphenols in HepG2 Cells

Hercog

Štern

Maisanaba

et al. 2020

Toxins

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Ever-expanding environmental pollution is causing a rise in cyanobacterial blooms and the accumulation of plastics in water bodies. Consequently, exposure to mixtures of cyanotoxins and plastic-related contaminants such as bisphenols (BPs) is of increasing concern. The present study describes genotoxic effects induced by co-exposure to one of the emerging cyanotoxins—cylindrospermopsin (CYN)—(0.5 µg/mL) and BPs (bisphenol A (BPA), S (BPS), and F (BPF); (10 µg/mL)) in HepG2 cells after 24 and 72 h of exposure. The cytotoxicity was evaluated with an MTS assay and genotoxicity was assessed through the measurement of the induction of DNA double strand breaks (DSB) with the γH2AX assay. The deregulation of selected genes (xenobiotic metabolic enzyme genes, DNA damage, and oxidative response genes) was assessed using qPCR. The results showed a moderate reduction of cell viability and induction of DSBs after 72 h of exposure to the CYN/BPs mixtures and CYN alone. None of the BPs alone reduced cell viability or induced DSBs. No significant difference was observed between CYN and CYN/BPs exposed cells, except with CYN/BPA, where the antagonistic activity of BPA against CYN was indicated. The deregulation of some of the tested genes (CYP1A1, CDKN1A, GADD45A, and GCLC) was more pronounced after exposure to the CYN/BPs mixtures compared to single compounds, suggesting additive or synergistic action. The present study confirms the importance of co-exposure studies, as our results show pollutant mixtures to induce effects different from those confirmed for single compounds.

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Section: Dna Damage Response Genesmentioning

confidence: 98%

Section: Xenobiotic Metabolism-cyp1a1mentioning

confidence: 99%

Plastics in Cyanobacterial Blooms—Genotoxic Effects of Binary Mixtures of Cylindrospermopsin and Bisphenols in HepG2 Cells

Hercog

Štern

Maisanaba

et al. 2020

Toxins

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show abstract

“…The biosynthesis relies on the function of CYP19a1, also called aromatase, performing the conversion from testosterone to estrogen [ 6 ]. The study found that the expression of CYP19a1 exists in different tissues in human, including liver, muscle, placenta, bone, breast, adipose tissue, and brain [ 7 , 8 ]. So, it is not surprised that the sites of estrogen production are widely distributed over the different human organs and tissues.…”

Section: Estrogen and Estrogen Receptormentioning

confidence: 99%

Estrogen/ER in anti-tumor immunity regulation to tumor cell and tumor microenvironment

Wang¹,

Jin

Qian

et al. 2021

Cancer Cell Int

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As the essential sexual hormone, estrogen and its receptor has been proved to participate in the regulation of autoimmunity diseases and anti-tumor immunity. The adjustment of tumor immunity is related to the interaction between cancer cells, immune cells and tumor microenvironment, all of which is considered as the potential target in estrogen-induced immune system regulation. However, the specific mechanism of estrogen-induced immunity is poorly understood. Typically, estrogen causes the nuclear localization of estrogen/estrogen receptor complex and alternates the transcription pattern of target genes, leading to the reprogramming of tumor cells and differentiation of immune cells. However, the estrogen-induced non-canonical signal pathway activation is also crucial to the rapid function of estrogen, such as NF-κB, MAPK-ERK, and β-catenin pathway activation, which has not been totally illuminated. So, the investigation of estrogen modulatory mechanisms in these two manners is vital for the tumor immunity and can provide the potential for endocrine hormone targeted cancer immunotherapy. Here, this review summarized the estrogen-induced canonical and non-canonical signal transduction pathway and aimed to focus on the relationship among estrogen and cancer immunity as well as immune-related tumor microenvironment regulation. Results from these preclinical researches elucidated that the estrogen-target therapy has the application prospect of cancer immunotherapy, which requires the further translational research of these treatment strategies.

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“…The clinical analysis suggests the potential impact of CYP19A1 in postmenopausal endocrine responsive breast cancer [37]. The study in vitro indicates that BPA induces cell proliferation and growth in human choriocarcinoma cell line [38]. As revead in computational assaus, the pharmacological functions of to treat BPA-related OS were identi ed accordingly, such as ossi cation, positive regulation of bone resorption, positive regulation of bone remodeling, regulation of in ammatory response, neuroin ammatory response, positive regulation of in ammatory response, interleukin-12 secretion, positive regulation of interleukin-12 production.…”

Section: Discussionmentioning

confidence: 95%

Bioinformatic Characteristics and Therapeutic Mechanisms of Calycosin-Anti-Bisphenol A-related Osteosarcoma

Tan

et al. 2020

Preprint

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BackgroundEnvironmentally, bisphenol A (BPA) is well-known as a pollutant caused human health risk, such as osteosarcoma (OS). OS, a deadly bone neoplasia, may occur in children and adults. Recently, the anti-OS pharmacotherapy prescribes limitedly. Interestingly, our previous experiments evidence that calycosin exerts the potential anti-OS action in vitro. Thus, in this report, we aimed to characterize and detail the therapeutic targets and mechanisms of calycosin-anti-BPA-related OS by means of network pharmacology and molecular docking analyses. ResultsIn details, the bioinformatic data revealed the mapped, core targets, biological functions, molecular pathways of calycosin to treat BPA-related OS. The computational analysis indicated that molecular docking ability and characteristic of core targets in calycosin to treat BPA-related OS were identified. Meanwhile, all optimal functions and pathways of calycosin-anti-BPA-related OS were revealed, as detailed in pathway networks. ConclusionsTaken together, the network pharmacology and structural biology findings illustrate the core biotargets, pharmacological functions and pathways of calycosin-anti-BPA-related OS. Potentially, these identified core targets may attribute to the scientific development of calycosin against BPA-related OS.

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Bisphenol A affects estradiol metabolism by targeting CYP1A1 and CYP19A1 in human placental JEG-3 cells

Cited by 30 publications

References 45 publications

Plastics in Cyanobacterial Blooms—Genotoxic Effects of Binary Mixtures of Cylindrospermopsin and Bisphenols in HepG2 Cells

Plastics in Cyanobacterial Blooms—Genotoxic Effects of Binary Mixtures of Cylindrospermopsin and Bisphenols in HepG2 Cells

Estrogen/ER in anti-tumor immunity regulation to tumor cell and tumor microenvironment

Bioinformatic Characteristics and Therapeutic Mechanisms of Calycosin-Anti-Bisphenol A-related Osteosarcoma

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