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Cancer Cell death Cell cycle Cytoskeleton Exo/endocytosis Differentiation Division Organelles Signalling Stem cells Trafficking
Cell Biology International (2009) 33, 239–246 (Printed in Great Britain)
Docetaxel/zoledronic acid combination triggers apoptosis synergistically through downregulating antiapoptotic Bcl-2 protein level in hormone-refractory prostate cancer cells
B. Karabuluta, C. Ertena, M.K. Gula, E. Cengiza, B. Karacaa, Y. Kucukzeybeka, G. Gorumlua, H. Atmacab, S. Uzunoglub, U.A. Sanlia, Y. Baranc and R. Uslua*
aDivision of Medical Oncology, Tulay Aktas Oncology Hospital, School of Medicine, Ege University, Bornova, Izmir, Turkey
bSection of Molecular Biology, Department of Biology, Faculty of Science and Arts, Celal Bayar University, Muradiye, Manisa, Turkey
cDepartment of Molecular Biology and Genetics, Faculty of Science, Izmir Institute of Technology, Urla, Izmir, Turkey


Abstract

Docetaxel, a semi-synthetic taxane analogue, is used effectively in the treatment of metastatic prostate cancer. Zoledronic acid, the most potent member of bisphosphonates, has shown pleiotropic anti-tumoral effects on prostate cancer cells. We have explored the possible additive/synergistic effects and the apoptotic pathways induced by combination treatment of docetaxel and zoledronic acid in hormone and drug refractory, PC-3 and DU-145 prostate cancer cells. Combination of docetaxel and zoledronic acid synergistically inhibits cell growth in PC-3 and DU-145 cells. Moreover, this effect was due to downregulation of antiapoptotic protein Bcl-2 in PC-3 and DU-145 cells. In conclusion, docetaxel/zoledronic acid combination is potentially a novel and effective approach for the treatment of prostate cancer.


Key words: Prostate cancer, PC-3, DU-145, Docetaxel, Zoledronic acid, Bcl-2.

*Corresponding author. Tel.: +90 232 390 39 06; fax: +90 232 374 73 21.


Received 8 July 2008/24 July 2008; accepted 29 November 2008

doi:10.1016/j.cellbi.2008.11.011


ISSN Print: 1065-6995
ISSN Electronic: 1095-8355
Published by Portland Press Limited on behalf of the International Federation for Cell Biology (IFCB)