Prystowsky, M., Feeney, K., Kawachi, N., Montagna, C., Willmott, M., Wasson, C., … Parish, J.
School of Cancer Sciences, University of Birmingham, Edgbaston, Birmingham, B15 2TT, UK, Department of Pathology, Albert Einstein College of Medicine and Montefiore Medical Center, USA, Departments of Genetics and Pathology, Albert Einstein College of Medicine, USA, School of Medicine, Emmanuel College, University of Cambridge, UK, Institute of Molecular and Cellular Biology, University of Leeds, UK, SULSA, School of Biology, University of St Andrews, UK.
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 atG2/M and an associated decrease in expression of particular genes required for passage through G2 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 G2 delay and mitotic defects. A loss of G2-specific Plk1 and Cyclin B1 expression and co-incident increase in p21Waf1/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.
… “Red LED illumination (CoolLED) and a CCD camera”…
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