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Cells 2014, 3(1), 53-78; doi:10.3390/cells3010053

When Good Turns Bad: Regulation of Invasion and Metastasis by ErbB2 Receptor Tyrosine Kinase

Unit of Cell Death and Metabolism, Danish Cancer Society Research Center, Danish Cancer Society, Strandboulevarden 49, DK-2100 Copenhagen, Denmark
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Received: 25 November 2013 / Revised: 14 January 2014 / Accepted: 20 January 2014 / Published: 27 January 2014
(This article belongs to the Special Issue Receptor Tyrosine Kinases)
View Full-Text   |   Download PDF [529 KB, 29 January 2014; original version 27 January 2014]   |  

Abstract

Overexpression and activation of ErbB2 receptor tyrosine kinase in breast cancer is strongly linked to an aggressive disease with high potential for invasion and metastasis. In addition to inducing very aggressive, metastatic cancer, ErbB2 activation mediates processes such as increased cancer cell proliferation and survival and is needed for normal physiological activities, such as heart function and development of the nervous system. How does ErbB2 activation make cancer cells invasive and when? Comprehensive understanding of the cellular mechanisms leading to ErbB2-induced malignant processes is necessary for answering these questions. Here we present current knowledge about the invasion-promoting function of ErbB2 and the mechanisms involved in it. Obtaining detailed information about the “bad” behavior of ErbB2 can facilitate development of novel treatments against ErbB2-positive cancers. View Full-Text
Keywords: cathepsin B; cathepsin L; matrix metalloprotease; p95 ErbB2; p21-activated protein kinase; transforming growth factor β cathepsin B; cathepsin L; matrix metalloprotease; p95 ErbB2; p21-activated protein kinase; transforming growth factor β
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MDPI and ACS Style

Brix, D.M.; Clemmensen, K.K.B.; Kallunki, T. When Good Turns Bad: Regulation of Invasion and Metastasis by ErbB2 Receptor Tyrosine Kinase. Cells 2014, 3, 53-78.

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