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Tumor Biology

, Volume 35, Issue 2, pp 1531–1538 | Cite as

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

  • Mehmet Korkmaz
  • Cigir Biray Avcı
  • Cumhur Gunduz
  • Duygu Aygunes
  • Burcu Erbaykent-Tepedelen
Research Article

Abstract

Animal and cell culture studies have showed that boron and its derivatives may 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.

Keywords

Prostate cancer Boron Pentaborate hTERT Actin polymerization Apoptosis 

Notes

Acknowledgments

We would like to thank the National Boron Research Institute, BOREN, for providing DPD. This research was supported with grants (2009-92 and 2010-91) from BAP projects by the Celal Bayar University.

Conflicts of interests

No competing interests are declared by any of the authors.

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Copyright information

© International Society of Oncology and BioMarkers (ISOBM) 2013

Authors and Affiliations

  1. 1.Department of Medical Biology, Faculty of MedicineCelal Bayar UniversityManisaTurkey
  2. 2.Department of Medical Biology, Faculty of MedicineEge UniversityIzmirTurkey
  3. 3.Department of Molecular Biology and Genetic, Faculty of Science and LetterAvrasya UniversityTrabzonTurkey

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