Different thresholds of ZEB1 are required for Ras-mediated tumour initiation and metastasis

Yongqing Liu, Xiaoqin Lu, Li Huang, Wei Wang, Guomin Jiang, Kevin C. Dean, Brian Clem, Sucheta Telang, Alfred B. Jenson, Miriam Cuatrecasas, Jason Chesney, Douglas S. Darling, Antonio Postigo () and Douglas C. Dean ()
Additional contact information
Yongqing Liu: Molecular Targets Program, James Brown Cancer Center, University of Louisville Health Sciences Center
Xiaoqin Lu: University of Louisville Health Sciences Center
Li Huang: University of Louisville Health Sciences Center
Wei Wang: University of Louisville Health Sciences Center
Guomin Jiang: University of Louisville Health Sciences Center
Kevin C. Dean: University of Louisville Health Sciences Center
Brian Clem: Molecular Targets Program, James Brown Cancer Center, University of Louisville Health Sciences Center
Sucheta Telang: Molecular Targets Program, James Brown Cancer Center, University of Louisville Health Sciences Center
Alfred B. Jenson: Molecular Targets Program, James Brown Cancer Center, University of Louisville Health Sciences Center
Miriam Cuatrecasas: Centro de Diagnóstico Biomédico (CDB) Hospital Clínic, University of Barcelona
Jason Chesney: Molecular Targets Program, James Brown Cancer Center, University of Louisville Health Sciences Center
Douglas S. Darling: Endodontics, and Dental Hygiene, University of Louisville
Antonio Postigo: Molecular Targets Program, James Brown Cancer Center, University of Louisville Health Sciences Center
Douglas C. Dean: Molecular Targets Program, James Brown Cancer Center, University of Louisville Health Sciences Center

Nature Communications, 2014, vol. 5, issue 1, 1-10

Abstract: Abstract Ras pathway mutation is frequent in carcinomas where it induces expression of the transcriptional repressor ZEB1. Although ZEB1 is classically linked to epithelial–mesenchymal transition and tumour metastasis, it has an emerging second role in generation of cancer-initiating cells. Here we show that Ras induction of ZEB1 is required for tumour initiation in a lung cancer model, and we link this function to repression Pten, whose loss is critical for emergence of cancer-initiating cells. These two roles for ZEB1 in tumour progression can be distinguished by their requirement for different levels of ZEB1. A lower threshold of ZEB1 is sufficient for cancer initiation, whereas further induction is necessary for tumour metastasis.

Date: 2014
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DOI: 10.1038/ncomms6660

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