The pathophysiology of epithelial-mesenchymal transition induced by transforming growth factor-beta in normal and malignant mammary epithelial cells.
The pathophysiology of epithelial-mesenchymal transition induced by transforming growth factor-beta in normal and malignant mammary epithelial cells.
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在正常和恶性乳腺上皮细胞中转化生长因子β引起的上皮 - 间质转变的病理生理。
DOI：
10.1007/s10911-010-9181-1
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发表时间：
2010-06
影响因子：
2.5
通讯作者：
Schiemann, William P.
中科院分区：
文献类型：
--
作者：
Taylor, Molly A.;Parvani, Jenny G.;Schiemann, William P.
关键词：
上皮-间充质转化（epithelial -mesenchymal transition， EMT）是驱动极化的、不动的乳腺上皮细胞（MECs）获得极性的、高度迁移的成纤维细胞样特征的重要过程。EMT是一个与正常组织发育和器官发生、组织重塑和伤口愈合相关的不可缺少的过程。与之形成鲜明对比的是，不适当的EMT再激活很容易导致各种人类病理的发展，特别是那些与组织纤维化和癌细胞侵袭和转移相关的病理，包括乳腺癌细胞的侵袭和转移。虽然转移毫无疑问是乳腺癌最致命的方面，也是与疾病复发相关的最突出特征，但EMT介导乳腺癌转移起始和消退的分子机制仍然知之甚少。转化生长因子-β (TGF-β)是一种多功能细胞因子，密切参与调节许多生理过程，包括细胞分化、体内平衡和EMT。此外，TGF-β在mec中也是一种强大的肿瘤抑制因子，其肿瘤发展最终将TGF-β转化为侵袭性晚期乳腺肿瘤的致癌细胞因子。最近的研究表明，EMT在乳腺癌进展过程中介导TGF-β的功能转化，提示TGF-β诱导的EMT靶向化疗可能为改善乳腺癌患者的转移性疾病提供新的途径。本文综述了TGF-β在正常和恶性mec中调控EMT过程中参与病理生理活动的分子、细胞和微环境因素。
Epithelial-mesenchymal transition (EMT) is an essential process that drives polarized, immotile mammary epithelial cells (MECs) to acquire apolar, highly migratory fibroblastoid-like features. EMT is an indispensable process that is associated with normal tissue development and organogenesis, as well as with tissue remodeling and wound healing. In stark contrast, inappropriate reactivation of EMT readily contributes to the development of a variety of human pathologies, particularly those associated with tissue fibrosis and cancer cell invasion and metastasis, including that by breast cancer cells. Although metastasis is unequivocally the most lethal aspect of breast cancer and the most prominent feature associated with disease recurrence, the molecular mechanisms whereby EMT mediates the initiation and resolution of breast cancer metastasis remains poorly understood. Transforming growth factor-β (TGF-β) is a multifunctional cytokine that is intimately involved in regulating numerous physiological processes, including cellular differentiation, homeostasis, and EMT. In addition, TGF-β also functions as a powerful tumor suppressor in MECs, whose neoplastic development ultimately converts TGF-β into an oncogenic cytokine in aggressive late-stage mammary tumors. Recent findings have implicated the process of EMT in mediating the functional conversion of TGF-β during breast cancer progression, suggesting that the chemotherapeutic targeting of EMT induced by TGF-β may offer new inroads in ameliorating metastatic disease in breast cancer patients. Here we review the molecular, cellular, and microenvironmental factors that contribute to the pathophysiological activities of TGF-β during its regulation of EMT in normal and malignant MECs.
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影响因子：
4.8
作者：
Allington, Tressa M.;Galliher-Beckley, Amy J.;Schiemann, William P.
通讯作者：
Schiemann, William P.
影响因子：
32.4
作者：
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通讯作者：
Sonenshein, GE
影响因子：
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作者：
Boyer, AS;Ayerinskas, II;Runyan, RB
通讯作者：
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影响因子：
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作者：
Bellovin, D. I.;Simpson, K. J.;Mercurio, A. M.
通讯作者：
Mercurio, A. M.
影响因子：
4.8
作者：
Bertran, Esther;Caja, Laia;Fabregat, Isabel
通讯作者：
Fabregat, Isabel