Targeted Inhibition of CD133+ Cells in Oral Cancer Cell Lines

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dc.contributor.authorDamek-Poprawa, M.
dc.contributor.authorVolgina, A.
dc.contributor.authorKorostoff, J.
dc.contributor.authorSollecito, T. P.
dc.contributor.authorBrose, M. S.
dc.contributor.authorO'Malley Jr., B. W.
dc.contributor.authorAkintoye, Sunday O.
dc.contributor.authorDirienzo, J. M.
dc.date2023-05-18T02:48:20.000
dc.date.accessioned2023-05-22T13:16:29Z
dc.date.available2023-05-22T13:16:29Z
dc.date.issued2011-05-01
dc.date.submitted2022-06-09T08:36:33-07:00
dc.description.abstractResistance to treatment and the appearance of secondary tumors in head and neck squamous cell carcinomas (HNSCC) have been attributed to the presence of cells with stem-cell-like properties in the basal layer of the epithelium at the site of the lesion. In this study, we tested the hypothesis that these putative cancer stem cells (CSC) in HNSCC could be specifically targeted and inhibited. We found that 9 of 10 head and neck tumor biopsies contained a subpopulation of cells that expressed CD133, an unusual surface-exposed membrane-spanning glycoprotein associated with CSC. A genetically modified cytolethal distending toxin (Cdt), from the periodontal pathogen Aggregatibacter actinomycetemcomitans , was conjugated to an anti-human CD133 monoclonal antibody (MAb). The Cdt-MAb complex preferentially inhibited the proliferation of CD133+ cells in cultures of established cell lines derived from HNSCC. Inhibition of the CD133+ cells was rate- and dose-dependent. Saturation kinetics indicated that the response to the Cdt-MAb complex was specific. Healthy primary gingival epithelial cells that are native targets of the wild-type Cdt were not affected. Analysis of these data provides a foundation for the future development of new therapies to target CSC in the early treatment of HNSCC. Abbreviations: Cdt, cytolethal distending toxin; CSC, cancer stem cells; HNSCC, head and neck squamous cell carcinoma; MAb, monoclonal antibody. © 2011 International & American Associations for Dental Research.
dc.identifier.urihttps://repository.upenn.edu/handle/20.500.14332/9198
dc.legacy.articleid1371
dc.legacy.fields10.1177/0022034510393511
dc.legacy.fulltexturlhttps://repository.upenn.edu/cgi/viewcontent.cgi?article=1371&context=dental_papers&unstamped=1
dc.source.beginpage638
dc.source.endpage645
dc.source.issue461
dc.source.issue5
dc.source.journalDepartmental Papers (Dental)
dc.source.journaltitleJournal of Dental Research
dc.source.peerreviewedtrue
dc.source.statuspublished
dc.source.volume90
dc.subject.otherActinobacillus actinomycetemcomitans
dc.subject.otherAnimals
dc.subject.otherAntibodies
dc.subject.otherMonoclonal
dc.subject.otherAntigens
dc.subject.otherCD
dc.subject.otherBacterial Toxins
dc.subject.otherCarcinoma
dc.subject.otherSquamous Cell
dc.subject.otherCell Line
dc.subject.otherTumor
dc.subject.otherCell Proliferation
dc.subject.otherGene Expression Regulation
dc.subject.otherNeoplastic
dc.subject.otherGlycoproteins
dc.subject.otherHumans
dc.subject.otherImmunotoxins
dc.subject.otherMice
dc.subject.otherMolecular Targeted Therapy
dc.subject.otherMouth Neoplasms
dc.subject.otherMutagenesis
dc.subject.otherSite-Directed
dc.subject.otherNeoplastic Stem Cells
dc.subject.otherPeptides
dc.subject.otherDentistry
dc.titleTargeted Inhibition of CD133+ Cells in Oral Cancer Cell Lines
dc.typeArticle
digcom.contributor.authorDamek-Poprawa, M.
digcom.contributor.authorVolgina, A.
digcom.contributor.authorKorostoff, J.
digcom.contributor.authorSollecito, T. P.
digcom.contributor.authorBrose, M. S.
digcom.contributor.authorO'Malley Jr., B. W.
digcom.contributor.authorAkintoye, Sunday O.
digcom.contributor.authorDirienzo, J. M.
digcom.identifierdental_papers/461
digcom.identifier.contextkey29628938
digcom.identifier.submissionpathdental_papers/461
digcom.typearticle
dspace.entity.typePublication
upenn.schoolDepartmentCenterDepartmental Papers (Dental)
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