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dc.contributor.authorPlatais, C.*
dc.contributor.authorRadhakrishnan, R.*
dc.contributor.authorEbensberger, S.N.*
dc.contributor.authorMorgan, Richard*
dc.contributor.authorLambert, D.W.*
dc.contributor.authorHunter, K.D.*
dc.date.accessioned2018-07-30T16:09:41Z
dc.date.available2018-07-30T16:09:41Z
dc.date.issued2018-07
dc.identifier.citationPlatais C, Radhakrishnan R, Ebensberger SN et al (2018) Targeting HOX-PBX interactions causes death in oral potentially malignant and squamous carcinoma cells but not normal oral keratinocytes. BMC Cancer. 18:723.en_US
dc.identifier.urihttp://hdl.handle.net/10454/16517
dc.descriptionYesen_US
dc.description.abstractBackground: High HOX gene expression has been described in many cancers, including oral squamous cell carcinoma and the functional roles of these genes are gradually being understood. The pattern of overexpression suggests that inhibition may be useful therapeutically. Inhibition of HOX protein binding to PBX cofactors by the use of synthetic peptides, such as HXR9, results in apoptosis in multiple cancers. Methods: Activity of the HOX-PBX inhibiting peptide HXR9 was tested in immortalised normal oral (NOK), potentially-malignant (PMOL) and squamous cell carcinoma (OSCC) cells, compared to the inactive peptide CXR9. Cytotoxicity was assessed by LDH assay. Expression of PBX1/2 and c-Fos was assessed by qPCR and western blotting. Apoptosis was assessed by Annexin-V assay. Results: PMOL and OSCC cells expressed PBX1/2. HOX-PBX inhibition by HXR9 caused death of PMOL and OSCC cells, but not NOKs. HXR9 treatment resulted in apoptosis and increased expression of c-Fos in some cells, whereas CXR9 did not. A correlation was observed between HOX expression and resistance to HXR9. Conclusion: Inhibition of HOX-PBX interactions causes selective apoptosis of OSCC/PMOL, indicating selective toxicity that may be useful clinically.en_US
dc.description.sponsorshipIntercalated Degree Scholarship from the Harry Bottom Trust; scholarship by Becas Chile, Comisión Nacional de Investigación Científica y Tecnológica de Chile (CONICYT), Grant 72160041en_US
dc.language.isoenen_US
dc.relation.isreferencedbyhttps://doi.org/10.1186/s12885-018-4622-0en_US
dc.rights© The Author(s). 2018 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.en_US
dc.subjectHOX genesen_US
dc.subjectOral canceren_US
dc.subjectOSCCen_US
dc.subjectPBXen_US
dc.subjectHXR9en_US
dc.subjectApoptosisen_US
dc.titleTargeting HOX-PBX interactions causes death in oral potentially malignant and squamous carcinoma cells but not normal oral keratinocytesen_US
dc.status.refereedYesen_US
dc.date.Accepted2018-06-20
dc.date.application2018-07-06
dc.typeArticleen_US
dc.type.versionpublished version paperen_US
refterms.dateFOA2018-07-30T16:09:45Z


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