title: EMT, cell plasticity and metastasis.
abstract: Carcinoma cells that are induced to suppress their epithelial features and upregulate mesenchymal gene expression programs acquire traits that promote an invasive and metastatic phenotype. This is achieved through the expression of a program termed the epithelial-to-mesenchymal transition (EMT)-a fundamental cell-biological process that plays key roles in embryogenesis and wound healing. Re-activation of the EMT during cancer promotes disease progression and enhances the metastatic phenotype by bestowing upon previously benign carcinoma cell traits such as migration, invasion, resistance to anoikis, chemoresistance and tumour-initiating potential. Herein, we discuss recent insights into the function of the EMT and cancer cell plasticity during cancer progression, with a focus on their role in promoting successful completion of the later stages of the metastatic cascade.
authors.affiliation: Garvan Institute of Medical Research, Darlinghurst, New South Wales, Australia. c.chaffer@garvan.org.au.
authors.forename: Christine L
authors.initials: CL
authors.lastname: Chaffer
authors.affiliation: Garvan Institute of Medical Research, Darlinghurst, New South Wales, Australia.
authors.forename: Beatriz P
authors.initials: BP
authors.lastname: San Juan
authors.affiliation: Garvan Institute of Medical Research, Darlinghurst, New South Wales, Australia.|The Kinghorn Cancer Centre, St Vincent's Hospital, University of New South Wales, Darlinghurst, NSW, Australia.
authors.forename: Elgene
authors.initials: E
authors.lastname: Lim
authors.affiliation: Whitehead Institute for Biomedical Research, Cambridge, MA, USA. weinberg@wi.mit.edu.|Department of Biology, Massachusetts Institute of Technology, Cambridge, MA, USA. weinberg@wi.mit.edu.|Massachusetts Institute of Technology Ludwig Center for Molecular Oncology, Cambridge, MA, USA. weinberg@wi.mit.edu.
authors.forename: Robert A
authors.initials: RA
authors.lastname: Weinberg
mesh_terms: D000818:Animals; D001943:Breast Neoplasms / Q000188:drug therapy / Q000473:pathology*; D000066670:Cell Plasticity / Q000187:drug effects / Q000502:physiology*; D058750:Epithelial-Mesenchymal Transition / Q000187:drug effects; D005260:Female; D006801:Humans; D009362:Neoplasm Metastasis
keywords: Cancer cell plasticity; EMT; Metastasis; Partial-EMT; Tumor-initiating cells (TICs)