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The EMT-activator Zeb1 is a key factor for cell plasticity and promotes metastasis in pancreatic cancer
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The EMT-activator Zeb1 is a key factor for cell plasticity and promotes metastasis in pancreatic cancer
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Journal Article
The EMT-activator Zeb1 is a key factor for cell plasticity and promotes metastasis in pancreatic cancer
2017
Overview
Metastasis is the major cause of cancer-associated death. Partial activation of the epithelial-to-mesenchymal transition program (partial EMT) was considered a major driver of tumour progression from initiation to metastasis. However, the role of EMT in promoting metastasis has recently been challenged, in particular concerning effects of the Snail and Twist EMT transcription factors (EMT-TFs) in pancreatic cancer. In contrast, we show here that in the same pancreatic cancer model, driven by Pdx1-cre-mediated activation of mutant
Kras
and
p53
(KPC model), the EMT-TF Zeb1 is a key factor for the formation of precursor lesions, invasion and notably metastasis. Depletion of
Zeb1
suppresses stemness, colonization capacity and in particular phenotypic/metabolic plasticity of tumour cells, probably causing the observed
in vivo
effects. Accordingly, we conclude that different EMT-TFs have complementary subfunctions in driving pancreatic tumour metastasis. Therapeutic strategies should consider these potential specificities of EMT-TFs to target these factors simultaneously.
Adding to the recent debate on the role of epithelial–mesenchymal transition (EMT) in cancer cell invasion and metastasis, Brabletz and colleagues show that the EMT-inducing transcription factor Zeb1 drives pancreatic tumorigenesis and metastasis.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ 13/1
/ 13/100
/ 13/44
/ 13/51
/ 13/89
/ 13/95
/ 64/60
/ 96/109
/ Animals
/ Epithelial-Mesenchymal Transition
/ Genetic Predisposition to Disease
/ Homeodomain Proteins - genetics
/ Humans
/ Mutation
/ Neoplasms, Experimental - genetics
/ Neoplasms, Experimental - metabolism
/ Neoplasms, Experimental - pathology
/ Nuclear Proteins - metabolism
/ Pancreatic Neoplasms - genetics
/ Pancreatic Neoplasms - metabolism
/ Pancreatic Neoplasms - pathology
/ Proto-Oncogene Proteins p21(ras) - genetics
/ Snail Family Transcription Factors - genetics
/ Snail Family Transcription Factors - metabolism
/ Twist-Related Protein 1 - genetics
/ Twist-Related Protein 1 - metabolism
