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https://www.selleckchem.com/products/vtp50469.html Introduction Alterations of the epigenome may influence cancer initiation and progression. At the cellular level, histones are key regulators of chromatin accessibility and gene transcription; thus, inhibition of histone deacetylase enzymes (HDACs) constitutes an attractive target for therapy. In this study, we investigated the effects of the HDAC inhibitor Entinostat on oral squamous cell carcinoma (OSCC). Materials and methods We tested the effects of Entinostat on OSCC cell lines. Cell viability and growth were analyzed using MTT assay. Cell cycle analysis, cell apoptosis, cancer stem cells (CSCs) content, and the concentration of reactive oxygen species (ROS) in OSCC tumor cells were assessed using flow cytometry. The expression of histones and cell cycle regulatory proteins were examined by western blot. Results Administration of Entinostat resulted in reduced proliferation of OSCC cells, followed by cell cycle arrest at the G0/G1 phase, as well as substantial tumor apoptosis. We also found an increase in ROS production and significant reductions in CSCs. We also found that Entinostat caused increased acetylation histones H3 or H4, and changes in the expression of cell cycle-associated proteins such as p21. Conclusion This study indicates that Entinostat is a potential novel therapeutic agent for OSCC by halting tumor proliferation, inducing cytotoxicity and intracellular ROS, and attacking the CSCs.SARS-CoV-2 has become a major global challenge. The virus infects host cells using its spike glycoprotein and has significantly higher infectivity and mortality rates among the aged population. Here, based on bioinformatic analysis, I provide evidence that some members of the upper respiratory tract (URT) commensal bacteria express viral spike glycoprotein-binding proteins. Based on this analysis and available data showing a decline in the population of these bacteria in the elderly, I propose that some URT commensa

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