title: Homeostatic Signaling by Cell-Cell Junctions and Its Dysregulation during Cancer Progression.
abstract: The transition of sessile epithelial cells to a migratory, mesenchymal phenotype is essential for metazoan development and tissue repair, but this program is exploited by tumor cells in order to escape the confines of the primary organ site, evade immunosurveillance, and resist chemo-radiation. In addition, epithelial-to-mesenchymal transition (EMT) confers stem-like properties that increase efficiency of colonization of distant organs. This review evaluates the role of cell-cell junctions in suppressing EMT and maintaining a quiescent epithelium. We discuss the conflicting data on junctional signaling in cancer and recent developments that resolve some of these conflicts. We focus on evidence from breast cancer, but include other organ sites where appropriate. Current and potential strategies for inhibition of EMT are discussed.
authors.affiliation: Department of Nature Medicine, Tianjin Medical University School of Pharmacy, Tianjin 300070, China. yuyang@tmu.edu.cn.
authors.forename: Yang
authors.initials: Y
authors.lastname: Yu
authors.affiliation: Department of Pharmacology, Southern Illinois University School of Medicine, Springfield, IL 62794, USA. relble2@siumed.edu.|Simmons Cancer Institute, Southern Illinois University School of Medicine, Springfield, IL 62794, USA. relble2@siumed.edu.
authors.forename: Randolph C
authors.initials: RC
authors.lastname: Elble
keywords: E-cadherin; EMT; PLEKHA7; adherens junctions; breast cancer; cancer stem cells; claudins; dissemination; human mammary epithelial cells; miR30b; tight junctions