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

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

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

11 Citations (Scopus)
3 Downloads (Pure)


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.

Original languageEnglish
Article numbere2640
Number of pages10
JournalScientific Reports
Publication statusPublished - 12 Sept 2013


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


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