Next Article in Journal / Special Issue
Epicardial Epithelial-to-Mesenchymal Transition in Heart Development and Disease
Previous Article in Journal
Cancer Risk and Eicosanoid Production: Interaction between the Protective Effect of Long Chain Omega-3 Polyunsaturated Fatty Acid Intake and Genotype
Previous Article in Special Issue
Hypoxia, Epithelial-Mesenchymal Transition, and TET-Mediated Epigenetic Changes
Open AccessReview

Homeostatic Signaling by Cell–Cell Junctions and Its Dysregulation during Cancer Progression

1
Department of Nature Medicine, Tianjin Medical University School of Pharmacy, Tianjin 300070, China
2
Department of Pharmacology, Southern Illinois University School of Medicine, Springfield, IL 62794, USA
3
Simmons Cancer Institute, Southern Illinois University School of Medicine, Springfield, IL 62794, USA
*
Author to whom correspondence should be addressed.
Academic Editors: David A. Brenner, Tatiana Kisseleva and Jonas Fuxe
J. Clin. Med. 2016, 5(2), 26; https://doi.org/10.3390/jcm5020026
Received: 18 December 2015 / Revised: 5 February 2016 / Accepted: 5 February 2016 / Published: 18 February 2016
(This article belongs to the Special Issue Epithelial-Mesenchymal Transition)
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. View Full-Text
Keywords: E-cadherin; EMT; dissemination; breast cancer; human mammary epithelial cells; adherens junctions; tight junctions; claudins; PLEKHA7; miR30b; cancer stem cells E-cadherin; EMT; dissemination; breast cancer; human mammary epithelial cells; adherens junctions; tight junctions; claudins; PLEKHA7; miR30b; cancer stem cells
Show Figures

Figure 1

MDPI and ACS Style

Yu, Y.; Elble, R.C. Homeostatic Signaling by Cell–Cell Junctions and Its Dysregulation during Cancer Progression. J. Clin. Med. 2016, 5, 26.

Show more citation formats Show less citations formats
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

1
Back to TopTop