Adipose levels of polybrominated diphenyl ethers and risk of breast cancer

Hurley, Susan; Reynolds, Peggy; Nelson, David; Jeffrey, Stefanie S.; Petreas, Myrto

doi:10.1007/s10549-011-1481-7

Cited by 46 publications

(36 citation statements)

References 19 publications

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“…Very few data have addressed the possible effects of PBDEs on breast cancer risk. One case-control study found no relationship between adipose PBDE concentrations and breast cancer risk, but the sample was small and the levels of PBDEs were measured around the time of diagnosis and, therefore, may not have represented lifetime exposure (Hurley et al, 2011). However, another case-control study conducted by Holmes et al (2014) suggests a possible association between breast cancer and BDE-47.…”

Section: Introductionmentioning

confidence: 99%

Different mechanisms of action of 2, 2’, 4, 4’‐tetrabromodiphenyl ether (BDE‐47) and its metabolites (5‐OH‐BDE‐47 and 6‐OH‐BDE‐47) on cell proliferation in OVCAR‐3 ovarian cancer cells and MCF‐7 breast cancer cells

Karpeta

Maniecka

Gregoraszczuk

2016

J of Applied Toxicology

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Data concerning the possible action of polybrominated diphenyl ethers (PBDEs) in hormone-dependent cancer are scarce. Some data showed that PBDEs may directly affect breast cancer cells formation and only one research showed increased proliferation of the OVCAR-3 cells, but the results are ambiguous and the mechanisms are not clear. There is growing evidence that not only parent compounds but also its metabolites may be involved in cancer development. The present study was, therefore, designed to determine the effect of BDE-47 and its metabolites (2.5 to 50 ng ml ) on proliferation (BrdU), cell-cycle genes (real-time PCR) and protein expression (Western blot), protein expression of oestrogen receptors (α β), extracellular signal-regulated kinases 1 and 2 (ERK1/2) and protein kinase Cα (PKCα) in OVCAR-3 ovarian and MCF-7 breast cancer cells. In OVCAR-3 cells, the parent compound stimulated cell proliferation by activating CDK1, CDK7, E2F1 and E2F2. Independent of time of exposure, BDE-47 had no effect on ERα and ERβ protein expression and ERK1/2 and PKCα phosphorylation. Metabolites had no effect on cell proliferation but increased both ERs protein expression and ERK1/2 and PKCα phosphorylation. In MCF-7 cells, the parent compound displayed no effect on cell proliferation but decreased ERα and increased ERβ protein expression with concomitant induction of PKCα phosphorylation. Both metabolites increased MCF-7 cell proliferation, ERK1/2 and PKCα phosphorylation and decreased ERα and ERβ protein expression.We suggest that studies concerning PBDEs with fewer bromine atoms should be continued to understand environmental links to different hormone-dependent cancers. Copyright © 2016 John Wiley & Sons, Ltd.

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Section: Introductionmentioning

confidence: 99%

Different mechanisms of action of 2, 2’, 4, 4’‐tetrabromodiphenyl ether (BDE‐47) and its metabolites (5‐OH‐BDE‐47 and 6‐OH‐BDE‐47) on cell proliferation in OVCAR‐3 ovarian cancer cells and MCF‐7 breast cancer cells

Karpeta

Maniecka

Gregoraszczuk

2016

J of Applied Toxicology

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“…However, currently there is no evidence whether PBDEs increase the risk of hormone‐dependent cancer in humans. Few data have addressed the possible effects of PBDEs on breast cancer risk and, to our knowledge, one case–control study found no relationship between adipose PBDE concentrations and breast cancer risk (Hurley et al ., ), whereas another case–control study conducted by Holmes et al () suggests a possible association between breast cancer and BDE‐47. Some in vitro studies have shown that PBDEs may directly affect MCF‐7 breast tumor cells by stimulating proliferation and inhibiting apoptosis (Kwiecińska et al, ; Li et al, ; Llabjani et al ., , ; Meerts et al ., ; Ukpebor et al ., ); however, no mechanism of action has been elucidated.…”

Section: Introductionmentioning

confidence: 95%

Differences in the mechanisms of action of BDE‐47 and its metabolites on OVCAR‐3 and MCF‐7 cell apoptosis

Karpeta

Gregoraszczuk

2016

J of Applied Toxicology

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Data concerning possible carcinogenic action of polybrominated diphenyl ethers (PBDEs) in hormone-dependent tissues are limited. Our earlier studies showed that 2,2',4,4'-tetrabromodiphenyl ether (BDE-47) stimulated OVCAR-3 and MCF-7 cell proliferation, while its hydroxylated metabolites (5-OH-BDE-47 and 6-OH-BDE-47) increased estrogen receptors protein expression and extracellular signal-regulated kinase 1/2 and protein kinase Cα phosphorylation in these cell lines. In addition to cell proliferative disorder, a failure in the regulation of apoptosis can also lead to the formation and development of tumors. Therefore, in the present study, we investigated the effect of BDE-47 and its metabolites (2.5-50 ng ml ) on the expression of apoptosis regulatory genes and proteins, caspase-8 and -9 activity and DNA fragmentation induced by extracellular signal-regulated kinase inhibitor (PD098059) and protein kinase Cα inhibitor (Gӧ 6976) in ovarian (OVCAR-3) and breast (MCF-7) cancer cells. In OVCAR-3 cells, BDE-47 upregulated expression of most of the investigated genes and increased protein expression of tumor necrosis factor (TNF)-α, TNF receptor 1, caspase-6, Bcl-xl and caspase-8 activity. Whereas in MCF-7 cells, BDE-47 resulted in the downregulation of most of the investigated genes, and decreased caspase-8 and -9 activity. In both OVCAR-3 and MCF-7 cells, the expression of most of the investigated genes were downregulated by metabolites. Exposure of OVCAR-3 cells to 5-OH-BDE-47 corresponded with a decrease in the protein expression of caspase-6, caspase-9 and Bcl-xl and treatment with 6-OH-BDE-47 decreased Bcl-xl and TNF receptor 1 expression in OVCAR-3 cells and caspase-9 expression in MCF-7 cells. Hydroxylated metabolites of BDE-47 have strong inhibitory effects on apoptosis in ovarian and breast tumor cells and thus should be considered potential carcinogens in hormone-dependent cancers. Copyright © 2016 John Wiley & Sons, Ltd.

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“…In fact, many studies examined PBDE concentrations in fat tissue to indicate PBDE pollution levels in biotic samples (Pulkrabová et al, 2009;Hurley et al, 2011;Roszko et al, 2013). However, most of these studies reported no association between PBDE concentrations and age/exposure time, suggesting that bioaccumulation of PBDE, in fat tissue still depends on exposure levels (Malarvannan et al, 2013;Verreault et al, 2009;Pulkrabová et al, 2009).…”

Section: Tablementioning

confidence: 99%

Changes of polybrominated diphenyl ether concentrations in ducks with background exposure level and time

Liu¹,

Chen²,

Zhao³

et al. 2015

Chemosphere

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h i g h l i g h t sWe conducted a semi-field experiment of ducks in an e-waste recycling site. PPBDEs increased in fat with time, but fluctuated in other tissues with exposure level. High brominated DE levels increased with time but low brominated DE fluctuated in fat. High brominated DEs seem to have longer half-lives than low brominated DEs in fat. a r t i c l e i n f o b s t r a c tTo reveal what degree bioaccumulation of polybrominated diphenyl ethers (PBDEs) depends on exposure time and other factors, we conducted a semi-field experiment for a year (June 2008-June 2009) in a village in an e-waste recycling site in Taizhou, China. Approximately one hundred of juvenile ducks (Anas domestica Linnaeus) were entrusted to a villager. The ducks lived and forged in a PBDE-polluted pond from the late March to the end of November. Fish and mudsnails that were heavily polluted by PBDEs were main food. In cold days (from December to the middle March), the ducks lived in the villager' house, and mainly fed on paddy, which contained lower concentrations of PBDEs than fish and mudsnails. The female ducks were sampled for PBDE analysis every three months. We found that the P PBDE concentrations in duck liver, muscle, lung and brain fluctuated greatly with the changes of exposure levels that were determined by the environment and diets, but the P PBDE concentrations in fat tissue increased successively with time. Congener analysis demonstrated that the successive increase in the P PBDE concentrations with time in fat tissue was due to the successive increase in concentrations, with large fluctuations of low brominated congeners. The results show that PBDE concentrations in liver, muscle, lung and brain tissues heavily depends on exposure levels rather than exposure time. In fat tissue, by contrast, PBDE concentrations (mainly high brominated congeners) slightly depends on exposure levels but heavily depend on time relative to other tissues, implying that high brominated congeners seem to have longer half-lives than low brominated congeners in fat tissue.

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Adipose levels of polybrominated diphenyl ethers and risk of breast cancer

Cited by 46 publications

References 19 publications

Different mechanisms of action of 2, 2’, 4, 4’‐tetrabromodiphenyl ether (BDE‐47) and its metabolites (5‐OH‐BDE‐47 and 6‐OH‐BDE‐47) on cell proliferation in OVCAR‐3 ovarian cancer cells and MCF‐7 breast cancer cells

Different mechanisms of action of 2, 2’, 4, 4’‐tetrabromodiphenyl ether (BDE‐47) and its metabolites (5‐OH‐BDE‐47 and 6‐OH‐BDE‐47) on cell proliferation in OVCAR‐3 ovarian cancer cells and MCF‐7 breast cancer cells

Differences in the mechanisms of action of BDE‐47 and its metabolites on OVCAR‐3 and MCF‐7 cell apoptosis

Changes of polybrominated diphenyl ether concentrations in ducks with background exposure level and time

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