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ZEB1 in Pancreatic Cancer
Department of General and Visceral Surgery, University of Freiburg, Hugstetter Straße 55, 79106 Freiburg, Germany
* Author to whom correspondence should be addressed.
Received: 30 June 2010; in revised form: 16 August 2010 / Accepted: 17 August 2010 / Published: 18 August 2010
Abstract: Pancreatic cancer is one of the most malignant human neoplasias. On the molecular level, epithelial-mesenchymal transition (EMT) has been demonstrated to contribute to the malignant phenotype of pancreatic cancer cells. ZEB1 is a transcriptional repressor that has been identified as an inducer of EMT. A negative feedback loop between ZEB1 and microRNA-200c has been shown to regulate this EMT induction in various models. With respect to pancreatic cancer, primary effects of EMT comprise increased local and distant tumor cell dissemination. Another recently described feature of the EMT is the acquisition of cancer stem cell traits. For pancreatic cancer cells, antagonism between ZEB1 and stemness-inhibiting micro-RNAs has been demonstrated to contribute to this process, providing experimental support for the migrating cancer stem cell (MCSC) hypothesis. ZEB1 has also been shown to be associated with drug resistance of pancreatic cancer cells. This article reviews the biological functions of ZEB1 with a focus on pancreatic cancer.
Keywords: pancreatic cancer; ZEB1; EMT; MCSC
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Cite This Article
MDPI and ACS Style
Wellner, U.; Brabletz, T.; Keck, T. ZEB1 in Pancreatic Cancer. Cancers 2010, 2, 1617-1628.
Wellner U, Brabletz T, Keck T. ZEB1 in Pancreatic Cancer. Cancers. 2010; 2(3):1617-1628.
Wellner, Ulrich; Brabletz, Thomas; Keck, Tobias. 2010. "ZEB1 in Pancreatic Cancer." Cancers 2, no. 3: 1617-1628.