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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Main Authors: Yang Yu, Randolph C. Elble
Format: Article
Language:English
Published: MDPI AG 2016-02-01
Series:Journal of Clinical Medicine
Subjects:
EMT
Online Access:http://www.mdpi.com/2077-0383/5/2/26
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spelling 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
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