首页> 美国卫生研究院文献>International Journal of Breast Cancer >Green Tea Catechin EGCG Suppresses PCB 102-Induced Proliferation in Estrogen-Sensitive Breast Cancer Cells
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Green Tea Catechin EGCG Suppresses PCB 102-Induced Proliferation in Estrogen-Sensitive Breast Cancer Cells

机译:绿茶儿茶素EGCG抑制PCB 102诱导的雌激素敏感性乳腺癌细胞的增殖

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摘要

The persistence of polychlorinated biphenyls (PCBs) in the environment is of considerable concern since they accumulate in human breast tissue and may stimulate the growth of estrogen-sensitive tumors. Studies have shown that EGCG from green tea can modify estrogenic activity and thus may act as a cancer chemopreventive agent. In the present study, we evaluated the individual and combined effects of PCB 102 and EGCG on cell proliferation using an estrogen-sensitive breast cancer cell line MCF-7/BOS. PCB 102 (1–10 μM) increased cell proliferation in a dose-dependent manner. Furthermore, the proliferative effects of PCB 102 were mediated by ERα and could be abrogated by the selective ERα antagonist MPP. EGCG (10–50 μM) caused a dose-dependent inhibition of PCB 102-induced cell proliferation, with nearly complete inhibition at 25 μM EGCG. The antiproliferative action of EGCG was mediated by ERβ and could be blocked by the ERβ-specific inhibitor PHTPP. In conclusion, EGCG suppressed the proliferation-stimulating activity of the environmental estrogen PCB 102 which may be helpful in the chemoprevention of breast cancer.
机译:多氯联苯(PCBs)在环境中的持久性备受关注,因为它们会积聚在人的乳房组织中,并可能刺激雌激素敏感性肿瘤的生长。研究表明,绿茶中的EGCG可以改变雌激素的活性,因此可以作为癌症的化学预防剂。在本研究中,我们使用雌激素敏感性乳腺癌细胞系MCF-7 / BOS评估了PCB 102和EGCG对细胞增殖的单独和联合作用。 PCB 102(1–10μM)以剂量依赖性方式增加细胞增殖。此外,PCB 102的增殖作用是由ERα介导的,并且可以被选择性ERα拮抗剂MPP消除。 EGCG(10–50μM)引起剂量依赖性抑制PCB 102诱导的细胞增殖,在25μμMEGCG下几乎完全抑制。 EGCG的抗增殖作用是由ERβ介导的,并可能被ERβ特异性抑制剂PHTPP阻断。总之,EGCG抑制了环境雌激素PCB 102的增殖刺激活性,这可能有助于乳腺癌的化学预防。

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