PUBLICATION
Metastatic Colonization Requires the Repression of the Epithelial-Mesenchymal Transition Inducer Prrx1
- Authors
- Ocaña, O.H., Córcoles, R., Fabra, A., Moreno-Bueno, G., Acloque, H., Vega, S.,Barrallo-Gimeno, A., Cano, A., Nieto, M.A.
- ID
- ZDB-PUB-160725-38
- Date
- 2012
- Source
- Cancer Cell 22(6): 709-724 (Journal)
- Registered Authors
- Barrallo Gimeno, Alejandro, Córcoles, Rebeca, Nieto, Angela, Ocaña, Oscar H., Vega, Sonia
- Keywords
- none
- MeSH Terms
-
- Middle Aged
- Homeodomain Proteins/genetics
- Homeodomain Proteins/metabolism
- Homeodomain Proteins/physiology*
- Humans
- PubMed
- 23201163 Full text @ Cancer Cell
Abstract
The epithelial-mesenchymal transition (EMT) is required in the embryo for the formation of tissues for which cells originate far from their final destination. Carcinoma cells hijack this program for tumor dissemination. The relevance of the EMT in cancer is still debated because it is unclear how these migratory cells colonize distant tissues to form macrometastases. We show that the homeobox factor Prrx1 is an EMT inducer conferring migratory and invasive properties. The loss of Prrx1 is required for cancer cells to metastasize in vivo, which revert to the epithelial phenotype concomitant with the acquisition of stem cell properties. Thus, unlike the classical EMT transcription factors, Prrx1 uncouples EMT and stemness, and is a biomarker associated with patient survival and lack of metastasis.
Genes / Markers
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Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
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