| ORIGINAL ARTICLE |
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| Year : 2018 | Volume
: 14
| Issue : 10 | Page : 576-582 |
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Trichostatin A induces apoptosis in oral squamous cell carcinoma cell lines independent of hyperacetylation of histones
Boonsil Jang1, Lee-Han Kim1, Seung-Youp Lee2, Kyung-Eun Lee3, Ji-Ae Shin1, Sung-Dae Cho1
1 Department of Oral Pathology, School of Dentistry, Institute of Oral Bioscience and Biodegradable Material, Chonbuk National University, Jeonju 561-756, Republic of Korea
2 Department of Orthodontics, School of Dentistry, Chonbuk National University, Jeonju 561-756, Republic of Korea
3 Department of Oral Medicine, School of Dentistry, Research Institute of Clinical Medicine of Chonbuk National University-Biomedical Research Institute, Chonbuk National University Hospital, Jeonju 561-712, Republic of Korea
Correspondence Address:
Sung-Dae Cho
Department of Oral Pathology, School of Dentistry, Institute of Oral Bioscience and Biodegradable Material, Chonbuk National University, Jeonju 561.756
Republic of Korea
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0973-1482.177220
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Aim of Study: To investigate the apoptotic event of trichostatin A (TSA) and its associated mechanism in oral squamous cell carcinoma (OSCC) lines.
Materials and Methods: HSC-3 and Ca9.22 cell lines were evaluated using a trypan blue exclusion assay, histone isolation, soft agar assay, live/dead assay, 4%,6-diamidino-2-phenylindole staining, JC-1 mitochondrial membrane potential (MMP) assay, and Western blot analysis to demonstrate the anticancer activity of TSA.
Results: TSA decreased OSCC cell viability and proliferation without affecting the histone acetylation. TSA-induced caspase-dependent or -independent apoptosis according to cell types, TSA enhanced the expression levels of Bim protein by dephosphorylating ERK1/2 pathway in HSC-3 cells. TSA also damaged MMP and increased cytosolic apoptosis-inducing factor (AIF) in Ca9.22 cells.
Conclusion: The present study suggests that TSA may be a potential anticancer drug candidate for the treatment of OSCC through the induction of apoptosis.
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