CD44 Upregulation in E-Cadherin-Negative Esophageal Cancers Results in Cell Invasion 英文参考文献.docVIP
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CD44 Upregulation in E-Cadherin-Negative Esophageal Cancers Results in Cell Invasion 英文参考文献
CD44UpregulationinE-Cadherin-NegativeEsophageal
CancersResultsinCellInvasion
Gre′goireF.LeBras1,GillianL.Allison1,NicoleF.Richards1,ShaziaS.Ansari1,M.KayWashington2,3,
ClaudiaD.Andl1,3,4
*
1DepartmentofSurgery,VanderbiltIngramCancerCenter,VanderbiltUniversity,Nashville,Tennessee,UnitedStatesofAmerica,2DepartmentsofPathology,Vanderbilt
Ingram Cancer Center, Vanderbilt University, Nashville, Tennessee, United States of America, 3Vanderbilt Ingram Cancer Center, Vanderbilt University, Nashville,
Tennessee, United States of America, 4Department of Cancer Biology, Vanderbilt Ingram Cancer Center, Vanderbilt University, Nashville, Tennessee, United States of
America
Abstract
E-cadherinisfrequentlylostduringepithelial-mesenchymaltransitionandtheprogressionofepithelialtumorigenesis.We
found a marker of epithelial-mesenchymal transition, CD44, upregulated in response to functional loss of E-cadherin in
esophageal cell lines and cancer. Loss of E-cadherin expression correlates with increased expression of CD44 standard
isoform.Usinganorganotypicreconstructmodel,weshowincreasedCD44expressioninareasofcellinvasionisassociated
withMMP-9attheleadingedge.Moreover,ActivinAincreasescellinvasionthroughCD44upregulationafterE-cadherin
loss.Takentogether,ourresultsprovidefunctionalevidenceofCD44upregulationinesophagealcancerinvasion.
Citation:LeBrasGF,AllisonGL,RichardsNF,AnsariSS,WashingtonMK,etal.(2011)CD44UpregulationinE-Cadherin-NegativeEsophagealCancersResultsin
CellInvasion.PLoSONE6(11):e27063.doi:10.1371/journal.pone.0027063
Editor:AdamI.Marcus,EmoryUniversity,UnitedStatesofAmerica
ReceivedJuly29,2011;AcceptedOctober10,2011;PublishedNovember1,2011
Copyright: ? 2011 Le Bras et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits
unrestricteduse,distribution,andreproductioninanymedium,providedtheoriginalauthorandsourcearecredited.
Funding: CDA is the recipient of a Research Scholar Award from the American Gastroe
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