Entinostat is a novel therapeutic agent to treat oral squamous cell carcinoma
dc.contributor.author | Marques, Ana Elizia M. | |
dc.contributor.author | Nascimento Filho, Carlos Henrique V. | |
dc.contributor.author | Marinho Bezerra, Thamara M. | |
dc.contributor.author | Guerra, Eliete N. S. | |
dc.contributor.author | Castilho, Rogerio M. | |
dc.contributor.author | Squarize, Cristiane H. | |
dc.date.accessioned | 2020-10-01T23:31:00Z | |
dc.date.available | WITHHELD_12_MONTHS | |
dc.date.available | 2020-10-01T23:31:00Z | |
dc.date.issued | 2020-09 | |
dc.identifier.citation | Marques, Ana Elizia M.; Nascimento Filho, Carlos Henrique V.; Marinho Bezerra, Thamara M.; Guerra, Eliete N. S.; Castilho, Rogerio M.; Squarize, Cristiane H. (2020). "Entinostat is a novel therapeutic agent to treat oral squamous cell carcinoma." Journal of Oral Pathology & Medicine 49(8): 771-779. | |
dc.identifier.issn | 0904-2512 | |
dc.identifier.issn | 1600-0714 | |
dc.identifier.uri | https://hdl.handle.net/2027.42/162762 | |
dc.description.abstract | IntroductionAlterations of the epigenome may influence cancer initiation and progression. At the cellular level, histones are key regulators of chromatin accessibility and gene transcription; thus, the 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 MethodsWe 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 cell (CSC) 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 was examined by Western blot.ResultsThe 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 found an increase in ROS production and significant reductions in CSCs. We also found that entinostat caused increased acetylation histone H3 and histone H4, and changes in the expression of cell cycle‐associated proteins such as p21.ConclusionThis 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. | |
dc.publisher | Wiley Periodicals, Inc. | |
dc.subject.other | apoptosis | |
dc.subject.other | cancer stem cells | |
dc.subject.other | epigenetics | |
dc.subject.other | HDAC inhibitor | |
dc.subject.other | oral cancer | |
dc.title | Entinostat is a novel therapeutic agent to treat oral squamous cell carcinoma | |
dc.type | Article | |
dc.rights.robots | IndexNoFollow | |
dc.subject.hlbsecondlevel | Dentistry | |
dc.subject.hlbtoplevel | Health Sciences | |
dc.description.peerreviewed | Peer Reviewed | |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/162762/2/jop13039.pdf | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/162762/1/jop13039_am.pdf | en_US |
dc.identifier.doi | 10.1111/jop.13039 | |
dc.identifier.source | Journal of Oral Pathology & Medicine | |
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dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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