Disodium pentaborate decahydrate (DPD) induced apoptosis by decreasing hTERT enzyme activity and disrupting F-actin organization of prostate cancer cells

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dc.contributor.authorKorkmaz M.
dc.contributor.authorAvcı C.B.
dc.contributor.authorGunduz C.
dc.contributor.authorAygunes D.
dc.contributor.authorErbaykent-Tepedelen B.
dc.date.accessioned2024-07-22T08:17:17Z
dc.date.available2024-07-22T08:17:17Z
dc.date.issued2014
dc.description.abstractAnimal and cell culture studies have showed that boron and its derivativesmay be promising anticancer agents in prostate cancer treatment. Thus, DU145 cells were treated with disodium pentaborate decahydrate (DPD) for 24, 48, and 72 h in order to investigate the inhibitor effect and mechanisms of DPD. Then, cell proliferation, telomerase enzyme activity, actin polymerization, and apoptosis were detected by WST-1 assay, qRT-PCR, immunofluorescence labeling, and flow cytometry, respectively. We found that DPD inhibited the growth of human prostate cancer cell line DU145 at the concentration of 3.5 mM for 24 h. Our results demonstrated that 7 mM of DPD treatment prevented the telomerase enzyme activity at the rate of 38%. Furthermore, DPD has an apoptotic effect on DU145 cells which were examined by labeling DNA breaks. With 7 mM of DPD treatment, 8, 14, and 41% of apoptotic cells were detected for 24, 48, and 72 h, respectively. Additionally, immunofluorescence labeling showed that the normal organization of actin filaments was disrupted in DPD-exposed cells, which is accompanied by the alteration of cell shape and by apoptosis in targeted cells. Taken together, the results indicate that DPD may exert its cytotoxicity at least partly by interfering with the dynamic properties of actin polymerization and decreasing the telomerase activity. Eventually, for the first time, the results of this study showed that DPD suppressed the activity of telomerase in DU145 cells, and therefore, we suggested that DPD could be an important agent for its therapeutic potential in the treatment of prostate cancer. © International Society of Oncology and BioMarkers (ISOBM) 2013.
dc.identifier.DOI-ID10.1007/s13277-013-1212-2
dc.identifier.issn10104283
dc.identifier.urihttp://akademikarsiv.cbu.edu.tr:4000/handle/123456789/17020
dc.language.isoEnglish
dc.publisherIOS Press BV
dc.subjectActins
dc.subjectAnimals
dc.subjectAntineoplastic Agents
dc.subjectApoptosis
dc.subjectBorates
dc.subjectCell Line, Tumor
dc.subjectCell Proliferation
dc.subjectFlow Cytometry
dc.subjectHumans
dc.subjectMale
dc.subjectProstatic Neoplasms
dc.subjectTelomerase
dc.subjectantineoplastic agent
dc.subjectboron derivative
dc.subjectdisodium pentaborate decahydrate
dc.subjectF actin
dc.subjectmessenger RNA
dc.subjecttelomerase
dc.subjecttelomerase reverse transcriptase
dc.subjectunclassified drug
dc.subjectactin filament
dc.subjectactin polymerization
dc.subjectantineoplastic activity
dc.subjectantiproliferative activity
dc.subjectapoptosis
dc.subjectarticle
dc.subjectcancer cell
dc.subjectcancer inhibition
dc.subjectcell migration
dc.subjectcell proliferation
dc.subjectcell size
dc.subjectcell viability
dc.subjectcontrolled study
dc.subjectcytotoxicity
dc.subjectDNA strand breakage
dc.subjectenzyme activity
dc.subjectenzyme inhibition
dc.subjectflow cytometry
dc.subjecthuman
dc.subjecthuman cell
dc.subjectimmunofluorescence
dc.subjectmale
dc.subjectmetastasis
dc.subjectpriority journal
dc.subjectprostate cancer
dc.subjectreverse transcription polymerase chain reaction
dc.subjectWST-1 assay
dc.titleDisodium pentaborate decahydrate (DPD) induced apoptosis by decreasing hTERT enzyme activity and disrupting F-actin organization of prostate cancer cells
dc.typeArticle

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