Bisphenol A exerts estrogenic effects by modulating CDK1/2 and p38 MAP kinase activity

Lee, Hee-Seok; Park, Eun-Jung; Oh, Jun Ho; Moon, Guiim; Hwang, Myung-Sil; Kim, Sang Yub; Shin, Min Ki; Koh, Young Ho; Suh, Jin Hyang; Kang, Hui Seung; Jeon, Ju‐Hong; Rhee, Gyu-Seek; Jiang, Hong

doi:10.1080/09168451.2014.921557

Cited by 36 publications

(23 citation statements)

References 28 publications

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“…An ion at m/z 244.1 was observed in the ESI-MS/MS spectrum of deprotonated BPA, [21,32] wileyonlinelibrary.com/journal/rcm A common product ion peak was obtained from both BPB and BPC. The peak corresponded to two isomeric ions (C 10 In addition, the [M-H-C 2 H 6 ] À ion was observed ( Fig. 2(d)).…”

Section: Fragmentation Of Bisphenols In Negative Ion Esi-msmentioning

confidence: 96%

Investigation on fragmentation pathways of bisphenols by using electrospray ionization Orbitrap mass spectrometry

Zhao

et al. 2016

Rapid Commun. Mass Spectrom.

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Section: Fragmentation Of Bisphenols In Negative Ion Esi-msmentioning

confidence: 96%

Investigation on fragmentation pathways of bisphenols by using electrospray ionization Orbitrap mass spectrometry

Zhao

et al. 2016

Rapid Commun. Mass Spectrom.

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“…Also, it is contained in the internal coatings of beverage and food cans and line water pipes [ 8 ] . Meanwhile, BPA has long been a health concern associated with serious and chronic conditions due to its potency as a crucial EDC having an estrogenic effect in the body and its widespread exposure [ 7,9–10 ] . Specifically, BPA was reported to have the potential to increase cancer risk [ 11 ] and to have cell proliferation effects in estrogen-dependent breast and ovarian cancer cells as in case of endogenous estrogen, 17β-estradiol (E2), which has been reported to be closely linked to the pathogenesis of some cancers occurring in the reproductive organs [ 9,12–13 ] .…”

Section: Introductionmentioning

confidence: 99%

Effects of bisphenol compounds on the growth and epithelial mesenchymal transition of MCF-7 CV human breast cancer cells

et al. 2017

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Bisphenol-A (BPA) has been considered as an endocrine disrupting chemical (EDC) because it can exert estrogenic properties. For bisphenol-S (BPS) and bisphenol-F (BPF) that are BPA analogs and substitutes, their risk to estrogen-dependent cancer has been reported rarely compared with the numerous cases of BPA. In this study, we examined whether BPA, BPS, and BPF can lead to the proliferation, migration, and epithelial mesenchymal transition (EMT) of MCF-7 clonal variant (MCF-7 CV) breast cancer cells expressing estrogen receptors (ERs). In a cell viability assay, BPA, BPS, and BPF significantly increased proliferation of MCF-7 CV cells compared to control (DMSO) as did 17β-estradiol (E2). In Western blotting assay, BPA, BPS, and BPF enhanced the protein expression of cell cycle progression genes such as cyclin D1 and E1. In addition, MCF-7 CV cells lost cell to cell contacts and acquired fibroblast-like morphology by the treatment of BPA, BPS, or BPF for 24 hours. In cell migration assay, BPA, BPS, and BPF accelerated the migration capability of MCF-7 CV cells as did E2. In relation with the EMT process, BPA, BPS, and BPF increased the protein expression ofN-cadherin, while they decreased the protein expression of E-cadherin. When BPA, BPS, and BPF were co-treated with ICI 182,780, an ER antagonist, proliferation effects were reversed, the expression of cyclin D1 and cyclin E1 was downregulated, and the altered cell migration and expression ofN-cadherin and E-cadherin by BPA, BPS, and BPF were restored to the control level. Thus, these results imply that BPS and BPF also have the risk of breast cancer progression as much as BPA in the induction of proliferation and migration of MCF-7 CV cells by regulating the protein expression of cell cycle-related genes and EMT markersvia the ER-dependent pathway.

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“…Our data demonstrated that melatonin was capable of suppressing BPA‐induced proliferation in ER + BC cells. We have known that BPA could mimic estrogen to form a complex with ER and then activate ERE, as well as the MAPK and PI3K/AKT signaling pathways . Here, we found that melatonin could abolish BPA‐elevated phosphorylation of ERK and AKT.…”

Section: Discussionmentioning

confidence: 66%

Melatonin inhibits the proliferation of breast cancer cells induced by bisphenol A via targeting estrogen receptor‐related pathways

et al. 2018

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BackgroundBackground: Bisphenol A (BPA) is an estrogen‐like chemical widely contained in daily supplies. There is evidence that environmental exposure to BPA could contribute to the development of hormone‐related cancers. As is reported in numerous studies, melatonin, an endogenous hormone secreted by the pineal gland, could markedly inhibit estrogen‐induced proliferation of breast cancer (BC) cells. In this study, we intended to reveal the effects of melatonin on BPA‐induced proliferation of estrogen receptor‐positive BC cells.MethodsMethods: We used methyl thiazolyl tetrazolium, luciferase reporter gene and western blotting assays to testify the effect of melatonin on BPA‐mediated proliferation of MCF‐7 and T47D cells.ResultsMethyl thiazolyl tetrazolium and colony formation assays showed that melatonin could significantly abolish BPA‐elevated cell proliferation. Meanwhile, BPA‐upregulated phosphorylation of ERK and AKT was decreased by melatonin treatment. Mechanistically, we found that BPA was capable of upregulating the protein levels of steroid receptor coactivators (SRC‐1, SRC‐3), as well as promoting the estrogen response element activity. However, the addition of melatonin could remarkably block the elevation of steroid receptor coactivators expression and estrogen response element activity triggered by BPA.ConclusionConclusions: Therefore, these results demonstrated that melatonin could abrogate BPA‐induced proliferation of BC cells. Therapeutically, melatonin could be regarded as a potential medication for BPA‐associated BC.

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Bisphenol A exerts estrogenic effects by modulating CDK1/2 and p38 MAP kinase activity

Cited by 36 publications

References 28 publications

Investigation on fragmentation pathways of bisphenols by using electrospray ionization Orbitrap mass spectrometry

Investigation on fragmentation pathways of bisphenols by using electrospray ionization Orbitrap mass spectrometry

Effects of bisphenol compounds on the growth and epithelial mesenchymal transition of MCF-7 CV human breast cancer cells

Melatonin inhibits the proliferation of breast cancer cells induced by bisphenol A via targeting estrogen receptor‐related pathways

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