Molecular mechanisms underlying proliferation and apoptosis in breast cancer MCF-7 cells induced by pentabrominated diphenyl ethers

被引:2
作者
Department of Environment Hygiene, Chongqing University of Medical Sciences, Chongqing, China [1 ]
机构
[1] Department of Environment Hygiene, Chongqing University of Medical Sciences, Chongqing
来源
Toxicol. Environ. Chem. | 2009年 / 4卷 / 665-670期
关键词
5-BDE; Bax; Bcl-2; MCF-7; cell;
D O I
10.1080/02772240802343370
中图分类号
学科分类号
摘要
The molecular mechanisms underlying proliferation and apoptosis induced by pentabrominated diphenyl ethers (5-BDE) through regulation of mRNA and protein expression of Bcl-2 and Bax was investigated using breast cancer MCF-7 cells. Human breast cancer MCF-7 cells were grown in DMEM medium, MTT assay was employed to investigate cell proliferation. RT-PCR and immunohistochemistry was performed to determine mRNA and protein expression of Bcl-2 and Bax. Within the range of 1 × 10-8-10-4mol L-1, polybrominated diphenyl ethers (PBDE) stimulated proliferation in MCF-7 cells in a concentration- and time-dependent manner. RT-PCR and immunohistochemistry analyses revealed that treatment with PBDE for 72 h resulted in increased mRNA and protein expression of Bcl-2 and inhibition of Bax. Evidence indicates that 5-BDE exerted estrogenic actions and stimulated proliferation in estrogen responsive breast cancer MCF-7 cells via up-regulation of Bcl-2 mRNA and protein expression. © 2009 Taylor & Francis.
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页码:665 / 670
页数:5
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共 13 条
  • [1] Choi M.N., Yoo S.D., Lee B.M., Toxicological characteristics of endocrine-disrupting chemicals: Developmental toxicity, carcinogenicity and mutagenicity, Journal of Toxicology and Environmental Health, B, 7, pp. 1-24, (2004)
  • [2] Clarke R., Hilakivi-Clarke L., Trock B., Breast cancer: Dietary and environmental oestrogens, Biologist, 48, pp. 21-6, (2001)
  • [3] Darnerud P.O., Eriksen G.S., Johannsson T., Larsen P.B., Viluksela M., Polybrominated diphenyl ethers: Occurrence, dietary exposure and toxicology, Environmental Health Perspectives, 109, SUPPL. 1, pp. 49-68, (2001)
  • [4] Derosa C., Richter P., Pohl H., Jones D.E., Environmental exposures that affect the endocrine system: Public health implications, Journal of Toxicology and Environmental Health B, 1, pp. 3-26, (1998)
  • [5] Gadd S.L., Hobbs G., Miller M.R., Acetaminophen-induced proliferation of estrogen-responsive breast cancer cells is associated with increases in c-myc RNA expression and NF-kappaB activity, Toxicological Sciences, 66, pp. 233-43, (2002)
  • [6] Hale R.C., la Guardia M.J., Harvey E.P., Gaylor M.O., Mainor T.M., Duff W.H., Flame retardants: Persistent pollutants in land-applied sludges, Nature, 412, 140, (2001)
  • [7] Hallgren S., Darnerud P.O., Polybrominated diphenyl ethers (PBDEs), polychlorinated biphenyls (PCBs) and chlorinated paraffins (CPs) in rats - testing interactions and mechanisms for thyroid hormone effects, Toxicology, 177, pp. 227-43, (2002)
  • [8] McKinney J.D., Waller C.L., Molecular determinants of hormone mimicry: Halogenated aromatic hydrocarbon environmental agents, Journal of Toxicology and Environmental Health B, 1, pp. 27-58, (1998)
  • [9] Meironyte D., Noren K., Bergman A., Analysis of polybrominated diphenyl ethers in Swedish human milk. A time-related trend study, 1972-1997, Journal of Toxicology and Environmental Health A, 58, pp. 329-41, (1999)
  • [10] Reed J.C., Bcl-2 and the regulation of programmed cell death, The Journal of Cell Biology, 124, pp. 1-6, (1994)