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Inhibition of Plk1 and Cyclin B1 expression results in panobinostat-induced G(2) delay and mitotic defects

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Michael Prystowsky, Katherine Feeney, Nicole Kawachi, Cristina Montagna, Michelle Willmott, Christopher Wasson, Maciej Antkowiak, Olivier Loudig, Joanna Parish

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Abstract

The development of clinically useful histone deacetylase inhibitors has expanded greatly. In a preclinical study, we showed that panobinostat (LBH589) inhibits cell cycle progression of human head and neck squamous cell carcinoma (HNSCC) cell lines at G(2)/M and an associated decrease in expression of particular genes required for passage through G(2) and mitosis. In this study we sought to analyse the mechanistic underpinnings of panobinostat-induced growth arrest. HNSCC cell lines were synchronised and progression through mitosis monitored. We demonstrate that panobinostat causes a marked G(2) delay and mitotic defects. A loss of G(2)-specific Plk1 and Cyclin B1 expression and co-incident increase in p21(Waf1/Cip1) expression is also shown. Furthermore, we show a significant loss of E2F1 recruitment to the promoters of these genes in response to panobinostat treatment. These data provide mechanistic evidence of panobinostat-induced cell cycle arrest and highlight its potential as a chemotherapeutic agent for HNSCC.

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Original languageEnglish
Article numbere2640
Number of pages10
JournalScientific Reports
Volume3
DOIs
Publication statusPublished - 12 Sep 2013

    Research areas

  • Histone deacetylase inhibitor, Carcinoma-cell lines, Gene-expression, Cancer cells, In-vitro, LBH589, Apoptosis, Polo, Head, P53

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