Homeostatic Signaling by Cell–Cell Junctions and Its Dysregulation during Cancer Progression
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 a...
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doaj-1e9e28ef14544fab92ba597afc2538d52020-11-24T23:19:42ZengMDPI AGJournal of Clinical Medicine2077-03832016-02-01522610.3390/jcm5020026jcm5020026Homeostatic Signaling by Cell–Cell Junctions and Its Dysregulation during Cancer ProgressionYang Yu0Randolph C. Elble1Department of Nature Medicine, Tianjin Medical University School of Pharmacy, Tianjin 300070, ChinaDepartment of Pharmacology, Southern Illinois University School of Medicine, Springfield, IL 62794, USAThe 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.http://www.mdpi.com/2077-0383/5/2/26E-cadherinEMTdisseminationbreast cancerhuman mammary epithelial cellsadherens junctionstight junctionsclaudinsPLEKHA7miR30bcancer stem cells |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Yang Yu Randolph C. Elble |
spellingShingle |
Yang Yu Randolph C. Elble Homeostatic Signaling by Cell–Cell Junctions and Its Dysregulation during Cancer Progression Journal of Clinical Medicine E-cadherin EMT dissemination breast cancer human mammary epithelial cells adherens junctions tight junctions claudins PLEKHA7 miR30b cancer stem cells |
author_facet |
Yang Yu Randolph C. Elble |
author_sort |
Yang Yu |
title |
Homeostatic Signaling by Cell–Cell Junctions and Its Dysregulation during Cancer Progression |
title_short |
Homeostatic Signaling by Cell–Cell Junctions and Its Dysregulation during Cancer Progression |
title_full |
Homeostatic Signaling by Cell–Cell Junctions and Its Dysregulation during Cancer Progression |
title_fullStr |
Homeostatic Signaling by Cell–Cell Junctions and Its Dysregulation during Cancer Progression |
title_full_unstemmed |
Homeostatic Signaling by Cell–Cell Junctions and Its Dysregulation during Cancer Progression |
title_sort |
homeostatic signaling by cell–cell junctions and its dysregulation during cancer progression |
publisher |
MDPI AG |
series |
Journal of Clinical Medicine |
issn |
2077-0383 |
publishDate |
2016-02-01 |
description |
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. |
topic |
E-cadherin EMT dissemination breast cancer human mammary epithelial cells adherens junctions tight junctions claudins PLEKHA7 miR30b cancer stem cells |
url |
http://www.mdpi.com/2077-0383/5/2/26 |
work_keys_str_mv |
AT yangyu homeostaticsignalingbycellcelljunctionsanditsdysregulationduringcancerprogression AT randolphcelble homeostaticsignalingbycellcelljunctionsanditsdysregulationduringcancerprogression |
_version_ |
1725577482377101312 |