Published in

MDPI, Cancers, 3(2), p. 1617-1628, 2010

DOI: 10.3390/cancers2031617

Links

Tools

Export citation

Search in Google Scholar

ZEB1 in pancreatic Cancer

Journal article published in 2010 by Ulrich Wellner ORCID, Thomas Brabletz, Tobias Keck ORCID
This paper is made freely available by the publisher.
This paper is made freely available by the publisher.

Full text: Download

Green circle
Preprint: archiving allowed
Green circle
Postprint: archiving allowed
Green circle
Published version: archiving allowed
Data provided by SHERPA/RoMEO

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.