Context-specific roles of EMT programmes in cancer cell dissemination

A mechanically active heterotypic E-cadherin/N-cadherin adhesion enables fibroblasts to drive cancer cell invasion

(2017) Anna Labernadie et al.   NATURE CELL BIOLOGY

EMT: 2016

(2016) M. Angela Nieto et al.   CELL

Plasticity between Epithelial and Mesenchymal States Unlinks EMT from Metastasis-Enhancing Stem Cell Capacity

(2016) Evelyne Beerling et al.   Cell Reports

Epithelial-to-mesenchymal transition is dispensable for metastasis but induces chemoresistance in pancreatic cancer

(2015) Xiaofeng Zheng et al.   NATURE

Epithelial-to-mesenchymal transition is not required for lung metastasis but contributes to chemoresistance

(2015) Kari R. Fischer et al.   NATURE

Distinct EMT programs control normal mammary stem cells and tumour-initiating cells

(2015) Xin Ye et al.   NATURE

A Switch in the Expression of Embryonic EMT-Inducers Drives the Development of Malignant Melanoma

(2013) Julie Caramel et al.   CANCER CELL

Poised Chromatin at the ZEB1 Promoter Enables Breast Cancer Cell Plasticity and Enhances Tumorigenicity

(2013) Christine L. Chaffer et al.   CELL

Metastatic Colonization Requires the Repression of the Epithelial-Mesenchymal Transition Inducer Prrx1

(2012) Oscar H. Ocaña et al.   CANCER CELL

Spatiotemporal Regulation of Epithelial-Mesenchymal Transition Is Essential for Squamous Cell Carcinoma Metastasis

(2012) Jeff H. Tsai et al.   CANCER CELL

EMT and Dissemination Precede Pancreatic Tumor Formation

(2012) Andrew D. Rhim et al.   CELL

A reciprocal repression between ZEB1 and members of the miR-200 family promotes EMT and invasion in cancer cells

(2008) Ulrike Burk et al.   EMBO REPORTS