Effects of decabrominated diphenyl ether (PBDE-209) in regulation of growth and apoptosis of breast, ovarian, and cervical cancer cells.
Effects of decabrominated diphenyl ether (PBDE-209) in regulation of growth and apoptosis of breast, ovarian, and cervical cancer cells.
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DOI：
10.1289/ehp.1104051
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发表时间：
2012-04
影响因子：
10.4
通讯作者：
Chen DJ
中科院分区：
文献类型：
--
作者：
Li ZH;Liu XY;Wang N;Chen JS;Chen YH;Huang JT;Su CH;Xie F;Yu B;Chen DJ
背景资料：多溴联苯醚（PBDEs）通常用于建筑材料，电子产品，塑料，聚氨酯泡沫和纺织品，是环境中发现的健康危害。目的：在这项研究中，我们调查了PBDE-209，十溴二苯醚，对乳腺癌，卵巢癌和宫颈癌细胞的生长和凋亡的调节，以及潜在的蛋白质改变的影响。研究方法：我们使用MCF-7和MCF-7/ADR（多药耐药MCF-7）乳腺癌细胞系、HeLa宫颈癌细胞系、OVCAR-3卵巢癌细胞系和正常CHO（中国仓鼠卵巢）细胞系，使用细胞活力、免疫荧光和流式细胞术测定来评估PBDE-209的影响。蛋白质印迹分析用于检测蛋白质表达的变化。为了评估PBDE-209对细胞凋亡的影响，我们使用了蛋白激酶Cα（PKCα）抑制剂Gö 6976、细胞外信号调节激酶（ERK）抑制剂PD 98059和他莫昔芬。结果如下：我们的数据表明，PBDE-209以剂量和时间依赖的方式增加了肿瘤细胞系和CHO细胞的活力和增殖。PBDE-209还通过诱导S期或G2/M期改变细胞周期分布。此外，PBDE-209在乳腺癌细胞系（MCF-7和MCF-7/ADR）中部分抑制了他莫昔芬诱导的细胞凋亡，但在所有细胞系中抑制了Gö 6976和PD 98059诱导的细胞凋亡。在分子水平上，PBDE-209增强了细胞系中PKCα和ERK 1/2的磷酸化。结论：我们的数据表明，PBDE-209能够促进来自女性生殖系统的各种癌细胞和正常卵巢CHO细胞的增殖。此外，它减少他莫昔芬，PKCα和ERK抑制诱导的细胞凋亡。最后，PBDE-209上调了肿瘤细胞和CHO细胞中PKCα和ERK 1/2蛋白的磷酸化。
Background: Polybrominated diphenyl ethers (PBDEs), commonly used in building materials, electronics, plastics, polyurethane foams, and textiles, are health hazards found in the environment. Objective: In this study we investigated the effects of PBDE-209, a deca-PBDE, on the regulation of growth and apoptosis of breast, ovarian, and cervical cancer cells as well as the underlying protein alterations. Methods: We used MCF-7 and MCF-7/ADR (multidrug-resistant MCF-7) breast cancer cell lines, the HeLa cervical cancer cell line, the OVCAR-3 ovarian cancer cell line, and the normal CHO (Chinese hamster ovary) cell line to assess the effects of PBDE-209 using cell viability, immunofluorescence, and flow cytometric assays. Western blot assays were used to detect changes in protein expression. To assess the effects of PBDE-209 on apoptosis, we used the protein kinase Cα (PKCα) inhibitor Gö 6976, the extracellular signal-regulated kinase (ERK) inhibitor PD98059, and tamoxifen. Results: Our data indicate that PBDE-209 increased viability and proliferation of the tumor cell lines and in CHO cells in a dose- and time-dependent manner. PBDE-209 also altered cell cycle distribution by inducing the S phase or G2/M phase. Furthermore, PBDE-209 partially suppressed tamoxifen-induced cell apoptosis in the breast cancer cell lines (MCF-7 and MCF-7/ADR) but suppressed Gö 6976- and PD98059-induced apoptosis in all cell lines. At the molecular level, PBDE-209 enhanced PKCα and ERK1/2 phosphorylation in the cell lines. Conclusions: Our data demonstrate that PBDE-209 is able to promote proliferation of various cancer cells from the female reproductive system and normal ovarian CHO cells. Furthermore, it reduced tamoxifen, PKCα, and ERK inhibition-induced apoptosis. Finally, PBDE-209 up-regulated phosphorylation of PKCα and ERK1/2 proteins in tumor cells and in CHO cells.
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影响因子：
10.4
作者：
Kuriyama SN;Talsness CE;Grote K;Chahoud I
通讯作者：
Chahoud I
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