Bisphenol A disruption promotes mammary tumor microenvironment via phenotypic cell polarization and inflammatory response

Ruiz, Thalles Fernando Rocha; Colleta, Simone Jacovaci; Santos, Diego Dias dos; Castro, N. F. C.; Cabral, Ágata Silva; Calmon, Marília Freitas; Rahal, Paula; Gil, Cristiane Damas; Girol, Ana Paula; Vilamaior, Patrícia Simone Leite; Leonel, Ellen Cristina Rivas; Taboga, Sebastião Roberto

doi:10.1002/cbin.12007

Cited by 3 publications

(2 citation statements)

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“…inflammatory responses, promoting tumor growth and inflammatory cell recruitment, thereby promoting a malignant phenotype 18 .…”

Section: Ruiz Et Al Found That Bisphenol a Toxicity Disruptsmentioning

confidence: 99%

Bisphenol A Effect on T regulatory and T helper 17 Related Cytokines in Female Mice

Thabet,

Badary,

Ibrahim

et al. 2024

Egyptian Journal of Medical Microbiology

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In recent years there has been increasing concern about the potential health effects of exposure to Bisphenol A, especially in pregnant women and their offspring. The potential health effects of BPA exposure have been studied extensively in animal models. There is evidence to suggest that exposure to this compound can have a range of adverse health effects, including reproductive and developmental malformations, metabolic disorders, and immune dysfunction. Objectives: To determine the effect of Bisphenol A consumption on regulatory T cells and Th17 cell-associated cytokines in female mice, as well as whether Bisphenol A exposure could cause abortion in pregnant mice. Methodology: The study included 60 female mice divided into four groups; each group contained 15 female mice. The first group is the control, nonpregnant female mice, which take water containing 1% ethanol. The second group, female mice who aren t pregnant, which given 5 mg/ml/kg of a BPA solution. The third group is a control group of pregnant female mice who take water containing 1% ethanol. The fourth group, pregnant female mice, were given 5 mg/ml/kg of BPA solution. At the end of the trial, blood samples were taken and serum concentrations of Il-10, TGF-beta, and IL-17 were measured using ELISA kits. Results: In both pregnant and non-pregnant female mice, the experimental group exposed to BPA had considerably lower levels of TGF-beta and -IL-10 than the control group. Simultaneously, the experimental group had significantly higher levels of IL-17 than the control group. There was also a substantial change in levels between non-pregnant and pregnant mice. Conclusion: BPA exposure during pregnancy can result in aberrant T reg. and Th 17 cell-related cytokines and abortion in female mice.

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“…inflammatory responses, promoting tumor growth and inflammatory cell recruitment, thereby promoting a malignant phenotype 18 .…”

Section: Ruiz Et Al Found That Bisphenol a Toxicity Disruptsmentioning

confidence: 99%

Bisphenol A Effect on T regulatory and T helper 17 Related Cytokines in Female Mice

Thabet,

Badary,

Ibrahim

et al. 2024

Egyptian Journal of Medical Microbiology

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“…Moreover, BPA exposure can lead to the activation of other signaling pathways, such as Akt/PI3K or JAK-STAT pathways, and to the abnormal regulation of p53 expression in breast cancer [ 5 , 45 ]. Furthermore, besides its effects on cancer cells, BPA has been reported to affect the properties of the tumor microenvironment and to alter immune surveillance, thereby potentially exerting additional detrimental effects on breast cancer progression [ 46 , 47 , 48 ].…”

Section: Introductionmentioning

confidence: 99%

Bisphenol-A in Drinking Water Accelerates Mammary Cancerogenesis and Favors an Immunosuppressive Tumor Microenvironment in BALB–neuT Mice

Focaccetti,

Nardozi,

Benvenuto

et al. 2024

IJMS

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Bisphenol-A (BPA), a synthetic compound ubiquitously present in the environment, can act as an endocrine disruptor by binding to both canonical and non-canonical estrogen receptors (ERs). Exposure to BPA has been linked to various cancers, in particular, those arising in hormone-targeted tissues such as the breast. In this study, we evaluated the effect of BPA intake through drinking water on ErbB2/neu-driven cancerogenesis in BALB–neuT mice, transgenic for a mutated ErbB2/neu receptor gene, which reproducibly develop carcinomas in all mammary glands. In this model, BPA accelerated mammary cancerogenesis with an increase in the number of tumors per mouse and a concurrent decrease in tumor-free and overall survival. As assessed by immunohistochemistry, BALB–neuT tumors were ER-negative but expressed high levels of the alternative estrogen receptor GPR30, regardless of BPA exposure. On the other hand, BPA exposure resulted in a marked upregulation of progesterone receptors in preinvasive tumors and of Ki67, CD31, and phosphorylated Akt in invasive tumors. Moreover, based on several infiltration markers of immune cells, BPA favored an immunosuppressive tumor microenvironment. Finally, in vitro cell survival studies performed on a cell line established from a BALB–neuT breast carcinoma confirmed that BPA’s impact on cancer progression can be particularly relevant after chronic, low-dose exposure.

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Interleukin-41 diminishes cigarette smoke-induced lung inflammation in mice

Cen,

Mai,

Jin

et al. 2023

International Immunopharmacology

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Bisphenol A disruption promotes mammary tumor microenvironment via phenotypic cell polarization and inflammatory response

Cited by 3 publications

References 50 publications

Bisphenol A Effect on T regulatory and T helper 17 Related Cytokines in Female Mice

Bisphenol A Effect on T regulatory and T helper 17 Related Cytokines in Female Mice

Bisphenol-A in Drinking Water Accelerates Mammary Cancerogenesis and Favors an Immunosuppressive Tumor Microenvironment in BALB–neuT Mice

Interleukin-41 diminishes cigarette smoke-induced lung inflammation in mice

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