PKNOX2 expression and regulation in the bone marrow mesenchymal stem cells of Fanconi anemia patients and healthy donors

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buir.contributor.authorKonu, Özlen
dc.citation.epage678en_US
dc.citation.issueNumber1en_US
dc.citation.spage669en_US
dc.citation.volumeNumber46en_US
dc.contributor.authorÇağnan, I.en_US
dc.contributor.authorCoşgun, E.en_US
dc.contributor.authorKonu, Özlenen_US
dc.contributor.authorUçkan, D.en_US
dc.contributor.authorGünel-Özcan, A.en_US
dc.date.accessioned2020-02-03T06:59:04Z
dc.date.available2020-02-03T06:59:04Z
dc.date.issued2019
dc.departmentDepartment of Molecular Biology and Geneticsen_US
dc.description.abstractHOX and TALE transcription factors are important regulators of development and homeostasis in determining cellular identity. Deregulation of this process may drive cancer progression. The aim of this study was to investigate the expression of these transcription factors in the bone marrow derived mesenchymal stem cells (BM-MSCs) of Fanconi anemia (FA) patients, which is a cancer-predisposing disease. Expression levels of HOX and TALE genes in BM-MSCs were obtained from FA patients and healthy donors by RT-qPCR and highly conserved expression levels were observed between patient and donor cells, except PKNOX2, which is a member of TALE class. PKNOX2 was significantly downregulated in FA cells compared to donors (P < 0.05). PKNOX2 expression levels did not change with diepoxybutane (DEB), a DNA crosslinking agent, in either donor or FA cells except one patient’s with a truncation mutation of FANCA. A difference of PKNOX2 protein level was not obtained between FA patient and donor BM-MSCs by western blot analysis. When human TGF-β1 (rTGF-β1) recombinant protein was provided to the cultures, PKNOX2 as well as TGF-β1 expression increased both in FA and donor BM-MSCs in a dose dependent manner. 5 ng/mL rTGF-β stimulation had more dominant effect on the gene expression of donor BM-MSCs compared to FA cells. Decreased PKNOX2 expression in FA BM-MSCs may provide new insights into the molecular pathophysiology of the disease and TGF-β1 levels of the microenvironment may be the cause of PKNOX2 downregulation.en_US
dc.identifier.doi10.1007/s11033-018-4522-zen_US
dc.identifier.issn0301-4851
dc.identifier.urihttp://hdl.handle.net/11693/52977
dc.language.isoEnglishen_US
dc.publisherSpringeren_US
dc.relation.isversionofhttps://dx.doi.org/10.1007/s11033-018-4522-zen_US
dc.source.titleMolecular Biology Reportsen_US
dc.subjectBone marrow mesenchymal stem cellsen_US
dc.subjectFanconi anemiaen_US
dc.subjectHOX genesen_US
dc.subjectPKNOX2en_US
dc.subjectTALE classen_US
dc.subjectTGF-β1en_US
dc.titlePKNOX2 expression and regulation in the bone marrow mesenchymal stem cells of Fanconi anemia patients and healthy donorsen_US
dc.typeArticleen_US

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