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dc.contributor.authorBalahmar, Reham M.
dc.contributor.authorBoocock, David J.
dc.contributor.authorCoveney, Clare
dc.contributor.authorRay, Sankalita
dc.contributor.authorVadakekolathu, Jayakumar
dc.contributor.authorRegad, Tarik
dc.contributor.authorAli, Selman
dc.contributor.authorSivasubramaniam, Shiva
dc.date.accessioned2019-01-14T14:28:35Z
dc.date.available2019-01-14T14:28:35Z
dc.date.issued2018-01-11
dc.identifier.citationBalahmar, R.M., et al. (2018). ‘Identification and characterisation of NANOG+/OCT-4high/SOX2+ doxorubicin-resistant stem-like cells from transformed trophoblastic cell lines’. Oncotarget, 9(6), pp. 7054-7065en
dc.identifier.issn1949-2553
dc.identifier.doi10.18632/oncotarget.24151
dc.identifier.urihttp://hdl.handle.net/10545/623288
dc.description.abstractTreatment of gestational trophoblastic diseases (GTD) involves surgery, radiotherapy and chemotherapy. Although, these therapeutic approaches are highly successful, drug resistance and toxicity remain a concern for high risk patients. This Chemoresistance has also been observed in the presence of cancer stem cells that are thought to be responsible for cases of cancer recurrence. In this study, we report the presence of previously unknown populations of trophoblastic stem-like cells (SLCs) that are resistant to the chemotherapeutic drug doxorubicin. We demonstrate that these populations express the stem cell markers NANOG and Sox2 and higher levels of OCT-4 (NANOG+/OCT-4high/SOX2+). Although chemoresistant, we show that the invasive capacity of these trophoblastic SLCs is significantly inhibited by doxorubicin treatment. To better characterise these populations, we also identified cellular pathways that are involved in SLCs-chemoresistance to doxorubicin. In summary, we provide evidence of the presence of NANOG+/OCT-4+/SOX2+ trophoblastic SLCs that are capable to contribute to the susceptibility to GTD and that may be involved in Chemoresistance associated with drug resistance and recurrence in high risk GTDs’ patients. We propose that targeting these populations could be therapeutically exploited for clinical benefit.
dc.description.sponsorshipministry of higher education of kingdom of Saudi Arabia (Funding reference: S10886).en
dc.language.isoenen
dc.publisherImpact Journalsen
dc.relation.urlhttp://www.oncotarget.com/fulltext/24151en
dc.rightsArchived with thanks to Oncotargeten
dc.subjecttrophoblasten
dc.subjectstem-like cells (SLCs)en
dc.subjectdoxorubicinen
dc.subjectembryonic stem cells (ESCs)en
dc.subjectchemoresistanceen
dc.titleIdentification and characterisation of NANOG+/ OCT-4<sup>high</sup>/SOX2+ doxorubicin-resistant stem-like cells from transformed trophoblastic cell linesen
dc.typeArticleen
dc.contributor.departmentNottingham Trent Universityen
dc.identifier.journalOncotargeten
dc.dateAccepted2018-01-02
refterms.dateFOA2019-02-28T18:03:45Z
html.description.abstractTreatment of gestational trophoblastic diseases (GTD) involves surgery, radiotherapy and chemotherapy. Although, these therapeutic approaches are highly successful, drug resistance and toxicity remain a concern for high risk patients. This Chemoresistance has also been observed in the presence of cancer stem cells that are thought to be responsible for cases of cancer recurrence. In this study, we report the presence of previously unknown populations of trophoblastic stem-like cells (SLCs) that are resistant to the chemotherapeutic drug doxorubicin. We demonstrate that these populations express the stem cell markers NANOG and Sox2 and higher levels of OCT-4 (NANOG+/OCT-4high/SOX2+). Although chemoresistant, we show that the invasive capacity of these trophoblastic SLCs is significantly inhibited by doxorubicin treatment. To better characterise these populations, we also identified cellular pathways that are involved in SLCs-chemoresistance to doxorubicin. In summary, we provide evidence of the presence of NANOG+/OCT-4+/SOX2+ trophoblastic SLCs that are capable to contribute to the susceptibility to GTD and that may be involved in Chemoresistance associated with drug resistance and recurrence in high risk GTDs’ patients. We propose that targeting these populations could be therapeutically exploited for clinical benefit.


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