2,2′,4,4′-Tetrabromodiphenyl ether promotes human neuroblastoma SH-SY5Y cells migration via the GPER/PI3K/Akt signal pathway

Pc, Tian; Hl, Wang; Gh, Chen; Luo, Qiong; Chen, Z; Wang, Y; Liu, YF

doi:10.1177/0960327115578974

Cited by 18 publications

(11 citation statements)

References 51 publications

(56 reference statements)

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“…However, studies on the effects of PBDEs and OH-PBDEs on GPER are very limited. To the best of our knowledge, there has only been one report, which showed that 2, 2ʹ, 4, 4ʹ-tetrabromodiphenyl ether (BDE-047) stimulated the migration of human neuroblastoma SH-SY5Y cells and that the activity was inhibited by a GPER antagonist (G15), suggesting the involvement of GPER ( Tian et al. 2016 ).…”

Section: Introductionmentioning

confidence: 99%

Hydroxylated Polybrominated Biphenyl Ethers Exert Estrogenic Effects via Non-Genomic G Protein–Coupled Estrogen Receptor Mediated Pathways

Cao

Ren

Yang

et al. 2018

Environ Health Perspect

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Background:Numerous studies have indicated the estrogenic effects of polybrominated diphenyl ethers (PBDEs) and hydroxylated PBDEs (OH-PBDEs). However, the previous mechanistic studies focused on their estrogenic effects through genomic transcriptional activation of estrogen receptors.Objective:The present study aimed to investigate the estrogenic effects of PBDEs and OH-PBDEs via nongenomic G protein–coupled estrogen receptor (GPER) pathways.Methods:The binding affinities of 12 PBDEs and 18 OH-PBDEs with GPER were determined by a fluorescence competitive binding assay in a human breast cancer cell line (SKBR3). Molecular docking was performed to simulate the interactions. Their activities on GPER pathways were investigated by detecting calcium mobilization and cyclic adenosine monophosphate (cAMP) accumulation in SKBR3 cells. The effects on SKBR3 cell migration were investigated using Boyden chamber and wound-healing assays.Results:Our results showed that 11 of the OH-PBDEs but none of the PBDEs bound to GPER directly. Relative binding affinities ranged from 1.3% to 20.0% compared to 17β-estradiol. Docking results suggested that the hydroxyl group played an essential role in the binding of OH-PBDEs to GPER by forming hydrogen bond interactions. Most of the OH-PBDEs activated subsequent GPER signaling pathways. Among them, 4ʹ-OH-BDE-049, 5ʹ-OH-BDE-099, and 3ʹ-OH-BDE-154 displayed the highest activity with lowest effective concentrations (LOECs) of 10–100 nM. These three OH-PBDEs also promoted SKBR3 cell migration via GPER pathways with LOECs of 0.1–1μM.Conclusion:OH-PBDEs could bind to GPER, activate the subsequent signaling pathways, and promote SKBR3 cell migration via GPER pathways. OH-PBDEs might exert estrogenic effects by a novel nongenomic mechanism involving the activation of GPER at nanomolar concentrations. https://doi.org/10.1289/EHP2387

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Section: Introductionmentioning

confidence: 99%

Hydroxylated Polybrominated Biphenyl Ethers Exert Estrogenic Effects via Non-Genomic G Protein–Coupled Estrogen Receptor Mediated Pathways

Cao

Ren

Yang

et al. 2018

Environ Health Perspect

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“…A lot of researchs conducted on neuronal cells indicated that MMP-9 was an essential role in a variety of disease models [ 19 – 21 ]. Therefore, the effects of stretch injury and sesamin pretreatment on the expression of MMP-9 were assessed using Western blot and RT-PCR analyses in the present study.Pretreatment with sesamin significantly decreased the overexpression of MMP-9 after stretch injury in SH-SY5Y cells, relative protein levels of MMP-9 were 3.205 ± 0.2658 versus 2.125 ± 0.2546, p = 0.0262, F = 1.09 (vehicle vs sesamin), and relative gene expression of MMP-9 decreased 30.3% (Fig.…”

Section: Resultsmentioning

confidence: 99%

Sesamin protects SH-SY5Y cells against mechanical stretch injury and promoting cell survival

Liu

Yang

et al. 2017

BMC Neurosci

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BackgroundSesamin is a well-known antioxidant extracted from sesame seeds that exhibits various curative effects. The present study investigated whether sesamin would protect neuroblastoma SH-SY5Y cells against mechanical stretch injury-induced increases in reactive oxygen species (ROS) and apoptosis. Additionally, the mechanisms underlying these actives were investigated. Following exposure to mechanical stretch injury, cells were incubated for further investigations. Lactate dehydrogenase and Cell Counting Kit-8 assays were used to assess cell viability, and a terminal deoxynucleotidyl transferase dUTP nick end labeling assay and flow cytometric analysis were performed to evaluate changes in mitochondrial membrane potential (ΔΨm). Furthermore, intracellular levels of ROS production were measured by 20, 70-dichlorofluorescein diacetate staining, the mRNA levels of matrix metallopeptidase 9 (MMP-9) were evaluated using real-time polymerase chain reaction analysis, and the determinations had also been made on related proteins by Western blot analysis.ResultsExposure to mechanical stretch injury significantly decreased cell viability but this decrease was attenuated by pretreatment with sesamin (50 μM). Sesamin also significantly inhibited mechanical stretch injury-induced increases in intracellular ROS production, attenuated declines in ΔΨm, diminished the expressions of pro-apoptotic proteins, and decreased cell apoptosis. Stretch injury increased Bax and cleaved caspase 3 levels, enhanced the gene expression of MMP-9, increased the phosphorylation levels of Akt, p38, and JNK and decreased Bcl-2 levels in the cells. However, pretreatment with sesamin reduced the mechanical stretch injury-induced overexpression of MMP-9.ConclusionsSesamin protected SH-SY5Y cells against stretch injury by attenuating increases in ROS levels and suppressing apoptosis. Accordingly, sesamin seems to be a potentially therapeutic agent in the treatment of traumatic brain injury.Electronic supplementary materialThe online version of this article (doi:10.1186/s12868-017-0378-8) contains supplementary material, which is available to authorized users.

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“…Several studies have revealed that BDE-47 could impair neuronal differentiation (17). BDE-47 could cause DNA damage mediated by oxidative stress, and increase the in vitro migration and invasion of human neuroblastoma cells (18–21). Because of the association between PBDEs and hormone levels in humans (22), the impact of PBDEs on hormone-dependent cancers has become a topic of interest.…”

Section: Introductionmentioning

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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2,2′,4,4′-Tetrabromodiphenyl ether promotes human neuroblastoma SH-SY5Y cells migration via the GPER/PI3K/Akt signal pathway

Cited by 18 publications

References 51 publications

Hydroxylated Polybrominated Biphenyl Ethers Exert Estrogenic Effects via Non-Genomic G Protein–Coupled Estrogen Receptor Mediated Pathways

Hydroxylated Polybrominated Biphenyl Ethers Exert Estrogenic Effects via Non-Genomic G Protein–Coupled Estrogen Receptor Mediated Pathways

Sesamin protects SH-SY5Y cells against mechanical stretch injury and promoting cell survival

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

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