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2
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3
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本文引用的文献

1
Nuclear translocation of the epidermal growth factor receptor family membrane tyrosine kinase receptors.表皮生长因子受体家族膜酪氨酸激酶受体的核转位
Clin Cancer Res. 2009 Nov 1;15(21):6484-9. doi: 10.1158/1078-0432.CCR-08-2813. Epub 2009 Oct 27.
2
Histone acetylation: where to go and how to get there.组蛋白乙酰化：何去何从及如何实现
Epigenetics. 2009 Apr 1;4(3):139-43. doi: 10.4161/epi.4.3.8484. Epub 2009 Apr 18.
3
ErbB2-mediated Src and signal transducer and activator of transcription 3 activation leads to transcriptional up-regulation of p21Cip1 and chemoresistance in breast cancer cells.ErbB2介导的Src及信号转导与转录激活因子3激活导致乳腺癌细胞中p21Cip1转录上调及化疗耐药。
Mol Cancer Res. 2009 Apr;7(4):592-600. doi: 10.1158/1541-7786.MCR-08-0316.
4
Activation of Stat3 by heregulin/ErbB-2 through the co-option of progesterone receptor signaling drives breast cancer growth.在这里调节蛋白/ErbB-2通过孕酮受体信号传导的共同作用激活Stat3，从而推动乳腺癌生长。
Mol Cell Biol. 2009 Mar;29(5):1249-65. doi: 10.1128/MCB.00853-08. Epub 2008 Dec 22.
5
The role of hormonal therapy in the management of hormonal-receptor-positive breast cancer with co-expression of HER2.激素疗法在HER2共表达的激素受体阳性乳腺癌治疗中的作用。
Nat Clin Pract Oncol. 2008 Sep;5(9):531-42. doi: 10.1038/ncponc1179. Epub 2008 Jul 8.
6
ErbB-2 induces the cyclin D1 gene in prostate epithelial cells in vitro and in vivo.ErbB-2在体外和体内均可诱导前列腺上皮细胞中的细胞周期蛋白D1基因。
Cancer Res. 2007 May 1;67(9):4364-72. doi: 10.1158/0008-5472.CAN-06-1898.
7
Progestin effects on breast cancer cell proliferation, proteases activation, and in vivo development of metastatic phenotype all depend on progesterone receptor capacity to activate cytoplasmic signaling pathways.孕激素对乳腺癌细胞增殖、蛋白酶激活以及转移表型的体内发展的影响均取决于孕激素受体激活细胞质信号通路的能力。
Mol Endocrinol. 2007 Jun;21(6):1335-58. doi: 10.1210/me.2006-0304. Epub 2007 Apr 17.
8
The role of extranuclear signaling actions of progesterone receptor in mediating progesterone regulation of gene expression and the cell cycle.孕激素受体的核外信号作用在介导孕激素对基因表达和细胞周期调控中的作用。
Mol Endocrinol. 2007 Feb;21(2):359-75. doi: 10.1210/me.2006-0337. Epub 2006 Nov 30.
9
Loss of Hsp90 association up-regulates Src-dependent ErbB2 activity.热休克蛋白90（Hsp90）结合的丧失会上调Src依赖的表皮生长因子受体2（ErbB2）活性。
Mol Cell Biol. 2007 Jan;27(1):220-8. doi: 10.1128/MCB.00899-06. Epub 2006 Oct 9.
10
A cell-type-specific transcriptional network required for estrogen regulation of cyclin D1 and cell cycle progression in breast cancer.雌激素调控乳腺癌细胞周期蛋白D1及细胞周期进程所需的细胞类型特异性转录网络。
Genes Dev. 2006 Sep 15;20(18):2513-26. doi: 10.1101/gad.1446006.

孕激素受体通过一种新的转录效应诱导 ErbB-2 核转位，促进乳腺癌生长：ErbB-2 作为 Stat3 共激活因子发挥作用。

Progesterone receptor induces ErbB-2 nuclear translocation to promote breast cancer growth via a novel transcriptional effect: ErbB-2 function as a coactivator of Stat3.

机构信息

Instituto de Biología y Medicina Experimental, CONICET, Vuelta de Obligado 2490, Buenos Aires C1428ADN, Argentina.

出版信息

Mol Cell Biol. 2010 Dec;30(23):5456-72. doi: 10.1128/MCB.00012-10. Epub 2010 Sep 27.

DOI:10.1128/MCB.00012-10
PMID:20876300
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2976427/
Abstract

Progesterone receptor (PR) and ErbB-2 bidirectional cross talk participates in breast cancer development. Here, we identified a new mechanism of the PR and ErbB-2 interaction involving the PR induction of ErbB-2 nuclear translocation and the assembly of a transcriptional complex in which ErbB-2 acts as a coactivator of Stat3. We also highlighted that the function of ErbB-2 as a Stat3 coactivator drives progestin-induced cyclin D1 promoter activation. Notably, PR is also recruited together with Stat3 and ErbB-2 to the cyclin D1 promoter, unraveling a new and unexpected nonclassical PR genomic mechanism. The assembly of the nuclear Stat3/ErbB-2 transcriptional complex plays a key role in the proliferation of breast tumors with functional PR and ErbB-2. Our findings reveal a novel therapeutic intervention for PR- and ErbB-2-positive breast tumors via the specific blockage of ErbB-2 nuclear translocation.

摘要

孕激素受体（PR）和 ErbB-2 双向交流参与乳腺癌的发生。在这里，我们发现了 PR 和 ErbB-2 相互作用的一个新机制，涉及 PR 诱导 ErbB-2 核转位以及形成转录复合物，其中 ErbB-2 作为 Stat3 的共激活因子。我们还强调，ErbB-2 作为 Stat3 共激活因子的功能驱动孕激素诱导的细胞周期蛋白 D1 启动子激活。值得注意的是，PR 也与 Stat3 和 ErbB-2 一起被招募到细胞周期蛋白 D1 启动子上，揭示了一种新的、出乎意料的非经典 PR 基因组机制。核 Stat3/ErbB-2 转录复合物的组装在具有功能性 PR 和 ErbB-2 的乳腺癌增殖中起着关键作用。我们的研究结果揭示了一种通过特异性阻断 ErbB-2 核转位治疗 PR 和 ErbB-2 阳性乳腺癌的新方法。