Adhesion of beta1 integrin to fibronectin regulates CAM-DR phenotype via p21(WAF1/cip1) in HL60 acute myeloid leukemia (AML) cells

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dc.contributor.authorCanpinar, Hande
dc.contributor.authorEsendagli, Gunes
dc.contributor.authorKansu, Emin
dc.contributor.authorOzcan, Aysen Gunel
dc.contributor.authorGuc, Dicle
dc.date.accessioned2020-06-25T17:44:48Z
dc.date.available2020-06-25T17:44:48Z
dc.date.issued2008
dc.descriptionEsendagli, Gunes/0000-0003-4865-2377;
dc.description.abstractAims: Drug resistance is a major obstacle for a successful cancer therapy. Cell adhesion mediated drug resistance (CAM-DR) is a novel type of drug resistance and generated via interaction of cancer cells with the microenvironment. In this study, CAM-DR phenotype was analyzed in HL60 acute myeloid leukemia (AML) cells. Materials and Methods: Fibronectin (FN) adherence of HL60 cells was tested by a colorimetric adhesion assay. Flow cytometry analyses were performed to evaluate doxorubicin-incluced apoptosis and to determine cell cycle status. Proliferation rate was evaluated by [H-3]-thymidine incorporation assay. Western blot and RTPCR were used for analysis of the factors involved in cell cycle control. Results: Binding of HL60 to FN via alpha 4 beta 1 and alpha 5 beta 1 integrins exerted a CAM-DR phenotype, which shows resistance to apoptosis triggered by doxorubicin. FN-adherent HL60 cells accumulated in the G(0)/G(1) phase of cell cycle and stopped proliferation. However, after detachment from FN, cells entered S phase, proliferated, and became sensitive to apoptosis. The analysis of the factors involved in the G(0)/G(1) cell cycle checkpoint showed that CAM-DR phenotype might be regulated mainly by p21(waf/cip). Conclusions: Here we showed that CAM-DR may also represent a reversible drug resistance mechanism that decreases apoptosis and causes growth arrest in AML blasts.en_US
dc.identifier.citationclosedAccessen_US
dc.identifier.endpage104en_US
dc.identifier.issn1300-0144
dc.identifier.issn1303-6165
dc.identifier.issue2en_US
dc.identifier.scopus2-s2.0-44149110940
dc.identifier.scopusqualityQ1
dc.identifier.startpage97en_US
dc.identifier.urihttps://hdl.handle.net/20.500.12587/4199
dc.identifier.volume38en_US
dc.identifier.wosWOS:000254702300001
dc.identifier.wosqualityN/A
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.language.isoen
dc.publisherTubitak Scientific & Technical Research Council Turkeyen_US
dc.relation.ispartofTurkish Journal Of Medical Sciences
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectapoptosisen_US
dc.subjectCAM-DRen_US
dc.subjectfibronectinen_US
dc.subjectcell cycleen_US
dc.titleAdhesion of beta1 integrin to fibronectin regulates CAM-DR phenotype via p21(WAF1/cip1) in HL60 acute myeloid leukemia (AML) cellsen_US
dc.typeArticle

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