Abstract

Introduction Active areas of research in head and neck squamous cell carcinoma (HNSCC) include the identification of novel targets, exploration of resistance mechanisms to current therapies, and identification of combination strategies. Recent progress in molecular biology and translational research has initiated an era of personalised medicine in head and neck clinical oncology. The genetic information defined by biomarker analysis in tumours and individuals is indispensable for the administration of molecular targeting agents. Carcinogenesis is determined by various epigenetic events, such as histone deacetylation. Inhibition of histone deacetylase enzymes (HDACs) has been well documented as an attractive target for the development of chemotherapeutic drugs. The purpose of this study was to investigate the effects of Entinostat, an HDAC inhibitor, on cell viability and cell cycle in oral squamous cell carcinoma (OSCC) cell lines. This is the first study analysing the effects of Entinostat on oral carcinoma. Material and methods The cell lines involved in the study were HN6, HN12 and HN13 of the OSCC, and NOK-SI, normal oral keratinocytes. Cell viability was determined by the MTT assay, in which cells were treated with Entinostat in different concentrations (µM) for 24 hour. In addition, the effect of Entinostat on the distribution of cells in the cell cycle was analysed using flow cytometry. Results and discussions Treatment with Entinostat showed a decrease of cell proliferation of OSCC cell lines. After 24 hours, a significant dose-dependent proliferation inhibition was seen in all cell lines (p Conclusion The results demonstrated that Entinostat is a promising treatment of OSCC cells because of its antiproliferative effects and by inducing tumour cells to the cell cycle arrested at G0/G1 phase, thus preventing the tumour progression. However, further studies in vitro and in vivo are required to confirm these effects.

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