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本文引用的文献

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Epithelial to mesenchymal transition contributes to drug resistance in pancreatic cancer.上皮-间质转化促进胰腺癌的耐药性。
Cancer Res. 2009 Jul 15;69(14):5820-8. doi: 10.1158/0008-5472.CAN-08-2819. Epub 2009 Jul 7.
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miR-200 regulates PDGF-D-mediated epithelial-mesenchymal transition, adhesion, and invasion of prostate cancer cells.miR-200 调节 PDGF-D 介导的前列腺癌细胞上皮-间充质转化、黏附和侵袭。
Stem Cells. 2009 Aug;27(8):1712-21. doi: 10.1002/stem.101.
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The canonical Notch signaling pathway: unfolding the activation mechanism.经典Notch信号通路:揭示激活机制
Cell. 2009 Apr 17;137(2):216-33. doi: 10.1016/j.cell.2009.03.045.
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Epithelial-mesenchymal transition: a cancer researcher's conceptual friend and foe.上皮-间质转化:癌症研究者亦敌亦友的概念。
Am J Pathol. 2009 May;174(5):1588-93. doi: 10.2353/ajpath.2009.080545. Epub 2009 Mar 26.
5
Acquisition of epithelial-mesenchymal transition phenotype of gemcitabine-resistant pancreatic cancer cells is linked with activation of the notch signaling pathway.吉西他滨耐药胰腺癌细胞上皮-间质转化表型的获得与Notch信号通路的激活有关。
Cancer Res. 2009 Mar 15;69(6):2400-7. doi: 10.1158/0008-5472.CAN-08-4312. Epub 2009 Mar 10.
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Let-7 and miR-200 microRNAs: guardians against pluripotency and cancer progression.Let-7和miR-200微小RNA:多能性和癌症进展的守护者。
Cell Cycle. 2009 Mar 15;8(6):843-52. doi: 10.4161/cc.8.6.7907. Epub 2009 Mar 22.
7
Exploitation of the Notch signaling pathway as a novel target for cancer therapy.将Notch信号通路作为癌症治疗新靶点的研究
Anticancer Res. 2008 Nov-Dec;28(6A):3621-30.
8
PDGF-D signaling: a novel target in cancer therapy.血小板衍生生长因子-D信号传导:癌症治疗中的一个新靶点。
Curr Drug Targets. 2009 Jan;10(1):38-41. doi: 10.2174/138945009787122914.
9
Dysregulation of Hedgehog, Wnt and Notch signalling pathways in breast cancer.乳腺癌中刺猬信号通路、Wnt信号通路和Notch信号通路的失调。
Histol Histopathol. 2009 Mar;24(3):385-98. doi: 10.14670/HH-24.385.
10
Transcriptional regulation of cell polarity in EMT and cancer.上皮-间质转化和癌症中细胞极性的转录调控
Oncogene. 2008 Nov 24;27(55):6958-69. doi: 10.1038/onc.2008.346.

Notch 信号通路在发育和肿瘤侵袭过程中的上皮-间充质转化(EMT)中的作用。

The role of Notch signaling pathway in epithelial-mesenchymal transition (EMT) during development and tumor aggressiveness.

机构信息

Department of Pathology, Karmanos Cancer Institute, Wayne State University, Detroit, MI 48201, USA.

出版信息

Curr Drug Targets. 2010 Jun;11(6):745-51. doi: 10.2174/138945010791170860.

DOI:10.2174/138945010791170860
PMID:20041844
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3084452/
Abstract

The Notch signaling pathway maintains a balance between cell proliferation and apoptosis, and thus it is believed that Notch signaling pathways may play an important role in the development and progression of several malignancies. However, the functions of Notch signaling in EMT are largely unknown. This mini review describes the role of Notch signaling pathway in EMT, and cataloging how its deregulation is involved in EMT and tumor aggressiveness. Further attempts have been made to summarize the role of several chemopreventive agents that could be useful for targeted inactivation of Notch signaling, and thus it may cause reversal of EMT, which could become a novel approach for cancer prevention and treatment.

摘要

Notch 信号通路在细胞增殖和凋亡之间维持平衡,因此人们认为 Notch 信号通路可能在多种恶性肿瘤的发生和发展中发挥重要作用。然而,Notch 信号在 EMT 中的功能在很大程度上是未知的。这篇迷你综述描述了 Notch 信号通路在 EMT 中的作用,并列出了其失调如何参与 EMT 和肿瘤侵袭性。进一步的尝试已经被用来总结几种化学预防剂的作用,这些化学预防剂可能对 Notch 信号的靶向失活有用,从而可能导致 EMT 的逆转,这可能成为癌症预防和治疗的新方法。