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他莫昔芬可促进雌激素阳性乳腺癌MCF-7细胞凋亡并抑制其侵袭。

Tamoxifen promotes apoptosis and inhibits invasion in estrogen‑positive breast cancer MCF‑7 cells.

作者信息

Li Wei, Shi Xingpeng, Xu Yan, Wan Jianmei, Wei Shaohua, Zhu Ran

机构信息

Department of General Surgery, Second Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215123, P.R. China.

Department of General Surgery, First Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215123, P.R. China.

出版信息

Mol Med Rep. 2017 Jul;16(1):478-484. doi: 10.3892/mmr.2017.6603. Epub 2017 May 18.

DOI:10.3892/mmr.2017.6603
PMID:28534964
Abstract

Tamoxifen (TAM) is the earliest non-steroidal antiestrogen drug, which has been widely used in endocrine therapy targeting breast cancer. The aim of the present study was to investigate the effect of TAM on the proliferation, apoptosis, migration and invasion of the estrogen‑positive (ER+) breast cancer cell line MCF‑7 in vitro, and elucidate its mechanisms. It was demonstrated that TAM suppressed proliferation, migration and invasion, and induced apoptosis in MCF‑7 cells. Further investigation revealed that the mitochondrial membrane potential and the amount of ATP were significantly decreased following the treatment of MCF‑7 cells with TAM. Mitochondria are an important source of reactive oxygen species (ROS) and they are also the target of ROS as well. In the present study, TAM promoted the formation of ROS in MCF‑7 cells. In conclusion, these results reveal the underlying mechanism by which TAM induces ER+ breast cancer cell apoptosis and inhibits invasion, thereby supporting the use of TAM in breast cancer treatment.

摘要

他莫昔芬(TAM)是最早使用的非甾体类抗雌激素药物,已广泛应用于针对乳腺癌的内分泌治疗。本研究的目的是探讨TAM对雌激素阳性(ER+)乳腺癌细胞系MCF-7体外增殖、凋亡、迁移和侵袭的影响,并阐明其作用机制。结果表明,TAM可抑制MCF-7细胞的增殖、迁移和侵袭,并诱导其凋亡。进一步研究发现,用TAM处理MCF-7细胞后,线粒体膜电位和ATP含量显著降低。线粒体是活性氧(ROS)的重要来源,也是ROS作用的靶点。在本研究中,TAM促进了MCF-7细胞中ROS的形成。总之,这些结果揭示了TAM诱导ER+乳腺癌细胞凋亡并抑制侵袭的潜在机制,从而支持TAM在乳腺癌治疗中的应用。

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Tamoxifen promotes apoptosis and inhibits invasion in estrogen‑positive breast cancer MCF‑7 cells.他莫昔芬可促进雌激素阳性乳腺癌MCF-7细胞凋亡并抑制其侵袭。
Mol Med Rep. 2017 Jul;16(1):478-484. doi: 10.3892/mmr.2017.6603. Epub 2017 May 18.
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