Cyclin K dependent regulation of Aurora B affects apoptosisand proliferation by induction of mitotic catastrophe inprostate cancer

• Verfasst von: Schecher, Sabrina [VerfasserIn]
• Verfasst von: Walter, Britta [VerfasserIn]
• Verfasst von: Falkenstein, Michael [VerfasserIn]
• Verfasst von: Macher-Göppinger, Stephan [VerfasserIn]
• Verfasst von: Hadaschik, Boris [VerfasserIn]
• Verfasst von: Duensing, Stefan [VerfasserIn]
• Verfasst von: Roth, Wilfried [VerfasserIn]
• Verfasst von: Tagscherer, Katrin [VerfasserIn]
• Titel: Cyclin K dependent regulation of Aurora B affects apoptosisand proliferation by induction of mitotic catastrophe inprostate cancer
• Verf.angabe: Sabrina Schecher, Britta Walter, Michael Falkenstein, Stephan Macher-Goeppinger, Philipp Stenzel, Kristina Krümpelmann, Boris Hadaschik, Sven Perner, Glen Kristiansen, Stefan Duensing, Wilfried Roth and Katrin E. Tagscherer
• E-Jahr: 2017
• Jahr: 3 July 2017
• Umfang: 12 S.
• Fussnoten: Gesehen am 17.04.2018
• Titel Quelle: Enthalten in: International journal of cancer
• Ort Quelle: Bognor Regis : Wiley-Liss, 1966
• Jahr Quelle: 2017
• Band/Heft Quelle: 141(2017), 8, Seite 1643-1653
• ISSN Quelle: 1097-0215
• DOI: doi:10.1002/ijc.30864
• Datenträger: Online-Ressource
• Sprache: eng
• Sach-SW: cyclin K
• Sach-SW: aurora B
• Sach-SW: mitotic catastrophe
• Sach-SW: apoptosis
• Sach-SW: prostate cancer
• K10plus-PPN: 1572063874

Abstract

Cyclin K plays a critical role in transcriptional regulation as well as cell development. However, the role of Cyclin K in prostatecancer is unknown. Here, we describe the impact of Cyclin K on prostate cancer cells and examine the clinical relevance ofCyclin K as a biomarker for patients with prostate cancer. We show that Cyclin K depletion in prostate cancer cells inducesapoptosis and inhibits proliferation accompanied by an accumulation of cells in the G2/M phase. Moreover, knockdown ofCyclin K causes mitotic catastrophe displayed by multinucleation and spindle multipolarity. Furthermore, we demonstrate aCyclin K dependent regulation of the mitotic kinase Aurora B and provide evidence for an Aurora B dependent induction ofmitotic catastrophe. In addition, we show that Cyclin K expression is associated with poor biochemical recurrence-free survivalin patients with prostate cancer treated with an adjuvant therapy. In conclusion, targeting Cyclin K represents a novel, promis-ing anti-cancer strategy to induce cell cycle arrest and apoptotic cell death through induction of mitotic catastrophe in pros-tate cancer cells. Moreover, our results indicate that Cyclin K is a putative predictive biomarker for clinical outcome andtherapy response for patients with prostate cancer.