Please use this identifier to cite or link to this item: https://doi.org/10.1038/cddis.2016.387
DC FieldValue
dc.titleNormalizing' the malignant phenotype of luminal breast cancer cells via alpha(v)beta(3)-integrin
dc.contributor.authorAbu-Tayeh, H
dc.contributor.authorWeidenfeld, K
dc.contributor.authorZhilin-Roth, A
dc.contributor.authorSchif-Zuck, S
dc.contributor.authorThaler, S
dc.contributor.authorCotarelo, C
dc.contributor.authorTan, T.Z
dc.contributor.authorThiery, J.P
dc.contributor.authorGreen, J.E
dc.contributor.authorKlorin, G
dc.contributor.authorSabo, E
dc.contributor.authorSleeman, J.P
dc.contributor.authorTzukerman, M
dc.contributor.authorBarkan, D
dc.date.accessioned2020-09-09T01:22:38Z
dc.date.available2020-09-09T01:22:38Z
dc.date.issued2016
dc.identifier.citationAbu-Tayeh, H, Weidenfeld, K, Zhilin-Roth, A, Schif-Zuck, S, Thaler, S, Cotarelo, C, Tan, T.Z, Thiery, J.P, Green, J.E, Klorin, G, Sabo, E, Sleeman, J.P, Tzukerman, M, Barkan, D (2016). Normalizing' the malignant phenotype of luminal breast cancer cells via alpha(v)beta(3)-integrin. Cell Death and Disease 7 (12) : e2491. ScholarBank@NUS Repository. https://doi.org/10.1038/cddis.2016.387
dc.identifier.issn20414889
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/174910
dc.description.abstractReestablishing tissue organization of breast cancer cells into acini was previously shown to override their malignant phenotype. In our study, we demonstrate that alpha(v)beta(3) integrin (Int-?v?3), previously shown to play a role in cancer progression, promoted differentiation and growth arrest of organoids derived from luminal A breast cancer cells grown in their relevant three-dimensional microenvironment. These organoids differentiated into normal-like acini resembling a benign stage of breast tissue. Likewise, we demonstrate that Int-?v?3 is selectively expressed in the epithelium of the benign stage of breast tissues, and is lost during the early stages of luminal A breast cancer progression. Notably, the organoids' reversion into normal-like acini was mediated by cancer luminal progenitor-like cells expressing both EpCAM high CD49f low CD24 + and Int-?v?3. Furthermore, downregulation of Notch4 expression and downstream signaling was shown to mediate Int-?v?3-induced reversion. Intriguingly, when luminal A breast cancer cells expressing Int-?v?3 were injected into a humanized mouse model, differentiated tumors developed when compared with that generated by control cells. Hence, our data suggest that promoting differentiation of luminal A breast cancer cells by signaling emanating from Int-?v?3 can potentially promote 'normalization' of their malignant phenotype and may prevent the malignant cells from progressing. © 2016 The Author (S).
dc.publisherNature Publishing Group
dc.sourceUnpaywall 20200831
dc.subjectalpha6 integrin
dc.subjectCD24 antigen
dc.subjectcyclin dependent kinase inhibitor 1A
dc.subjectepithelial cell adhesion molecule
dc.subjectNotch4 receptor
dc.subjectvitronectin receptor
dc.subjectNotch receptor
dc.subjectNOTCH4 protein, human
dc.subjectoncoprotein
dc.subjectvitronectin receptor
dc.subjectanimal experiment
dc.subjectanimal model
dc.subjectapoptosis
dc.subjectArticle
dc.subjectbasement membrane
dc.subjectbreast cancer cell line
dc.subjectbreast carcinoma
dc.subjectbreast epithelium
dc.subjectbreast hyperplasia
dc.subjectcancer growth
dc.subjectcancer staging
dc.subjectcell differentiation
dc.subjectcell proliferation
dc.subjectcontrolled study
dc.subjectcytoplasm
dc.subjectdown regulation
dc.subjecthuman
dc.subjecthuman tissue
dc.subjectintraductal carcinoma
dc.subjectluminal A breast cancer
dc.subjectmouse
dc.subjectnonhuman
dc.subjectnuclear size
dc.subjectphenotype
dc.subjectpriority journal
dc.subjectprotein expression
dc.subjectprotein localization
dc.subjectthree dimensional imaging
dc.subjecttumor differentiation
dc.subjecttumor microenvironment
dc.subjectacinar cell
dc.subjectbreast tumor
dc.subjectcancer stem cell
dc.subjectcytoplasm
dc.subjectembryonic stem cell
dc.subjectfemale
dc.subjectgene silencing
dc.subjecthyperplasia
dc.subjectMCF-7 cell line
dc.subjectmetabolism
dc.subjectmulticellular spheroid
dc.subjectpathology
dc.subjectphenotype
dc.subjectsignal transduction
dc.subjectteratoma
dc.subjecttumor cell line
dc.subjectAcinar Cells
dc.subjectBasement Membrane
dc.subjectBreast Neoplasms
dc.subjectCell Differentiation
dc.subjectCell Line, Tumor
dc.subjectCell Proliferation
dc.subjectDown-Regulation
dc.subjectEmbryonic Stem Cells
dc.subjectFemale
dc.subjectGene Knockdown Techniques
dc.subjectHumans
dc.subjectHyperplasia
dc.subjectIntegrin alphaVbeta3
dc.subjectMCF-7 Cells
dc.subjectNeoplastic Stem Cells
dc.subjectOrganoids
dc.subjectPhenotype
dc.subjectProto-Oncogene Proteins
dc.subjectReceptors, Notch
dc.subjectSignal Transduction
dc.subjectSpheroids, Cellular
dc.subjectTeratoma
dc.typeArticle
dc.contributor.departmentCANCER SCIENCE INSTITUTE OF SINGAPORE
dc.contributor.departmentDEPT OF BIOCHEMISTRY
dc.description.doi10.1038/cddis.2016.387
dc.description.sourcetitleCell Death and Disease
dc.description.volume7
dc.description.issue12
dc.description.pagee2491
Appears in Collections:Elements
Staff Publications

Show simple item record
Files in This Item:
File Description SizeFormatAccess SettingsVersion 
10_1038_cddis_2016_387.pdf4.61 MBAdobe PDF

OPEN

NoneView/Download

SCOPUSTM   
Citations

10
checked on Feb 19, 2021

Page view(s)

33
checked on Feb 19, 2021

Google ScholarTM

Check

Altmetric


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.