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Growth-suppressive effect of suberoylanilide hydroxamic acid (SAHA) on human oral cancer cells

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dc.contributor.authorJang, Boonsil-
dc.contributor.authorShin, Ji-Ae-
dc.contributor.authorKim, Yong-Soo-
dc.contributor.authorKim, Ji-Young-
dc.contributor.authorYi, Ho-Keun-
dc.contributor.authorPark, Il-Song-
dc.contributor.authorCho, Nam-Pyo-
dc.contributor.authorCho, Sung-Dae-
dc.date.accessioned2024-08-08T01:37:17Z-
dc.date.available2024-08-08T01:37:17Z-
dc.date.created2024-08-07-
dc.date.created2024-08-07-
dc.date.issued2016-02-
dc.identifier.citationCellular Oncology, Vol.39 No.1, pp.79-87-
dc.identifier.issn2211-3428-
dc.identifier.urihttps://hdl.handle.net/10371/207001-
dc.description.abstractPurpose The histone deacetylase (HDAC) inhibitor suberoylanilide hydroxamic acid (SAHA) has been reported to exhibit anticancer activities in various cancer cell types, but as yet there are few reports on the anticancer effects of SAHA in oral squamous cell carcinoma (OSCC)-derived cells and xenograft models. Methods The anti-proliferative and apoptotic activities of SAHA were assessed in human HSC-3 and HSC-4 (OSCC)-derived cell lines and JB6 normal mouse skin-derived epidermal cells using histone acetylation, soft agar colony formation, trypan blue exclusion, 4'-6-diamidino-2-phenylindole (DAPI) staining, Live/Dead viability/cytotoxicity and Western blot analyses. Results We found that SAHA treatment resulted in hyperacetylation of histones H2A and H3 and a concomitant decrease in the viability of HSC-3 and HSC-4 cells. SAHA also significantly inhibited the neoplastic transformation of JB6 cells treated with TPA, whereas the viability of these cells was not affected by this treatment. Additionally, we found that SAHA suppressed the anchorage-independent growth (colony forming capacity in soft agar) of HSC-3 and HSC-4 cells. DAPI staining, Live/Dead and Western blot analyses revealed that SAHA can induce caspase-dependent apoptosis in HSC-3 and HSC-4 cells. We also found that SAHA treatment led to inhibition of ERK phosphorylation, and that two MEK inhibitors potentiated SAHA-mediated apoptosis. Okadaic acid treatment inhibited SAHA-mediated apoptosis in both the HSC-3 and HSC-4 cell lines, wheras SAHA induced a profound in vivo inhibition of tumor growth in HSC-3 xenografts. Conclusions Our results indicate that the ERK signaling pathway may constitute a critical denominator of SAHA-induced apoptosis in OSCC-derived cells and that SAHA may have therapeutic potential for OSCC.-
dc.language영어-
dc.publisherSpringer Verlag-
dc.titleGrowth-suppressive effect of suberoylanilide hydroxamic acid (SAHA) on human oral cancer cells-
dc.typeArticle-
dc.identifier.doi10.1007/s13402-015-0255-3-
dc.citation.journaltitleCellular Oncology-
dc.identifier.wosid000368732600008-
dc.identifier.scopusid2-s2.0-84955411158-
dc.citation.endpage87-
dc.citation.number1-
dc.citation.startpage79-
dc.citation.volume39-
dc.description.isOpenAccessN-
dc.contributor.affiliatedAuthorCho, Sung-Dae-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.subject.keywordPlusHISTONE DEACETYLASE INHIBITOR-
dc.subject.keywordPlusIN-VITRO-
dc.subject.keywordPlusINDUCED APOPTOSIS-
dc.subject.keywordPlusEXPRESSION-
dc.subject.keywordPlusCARCINOMA-
dc.subject.keywordPlusVORINOSTAT-
dc.subject.keywordPlusDEATH-
dc.subject.keywordPlusMECHANISMS-
dc.subject.keywordPlusPATHWAY-
dc.subject.keywordAuthorSaha-
dc.subject.keywordAuthorOral cancer-
dc.subject.keywordAuthorApoptosis-
dc.subject.keywordAuthorERK-
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  • School of Dentistry
  • Department of Dentistry
Research Area Discovery of molecular targets related to oral cancer metastasis and identification of signal transduction system, Identifying the role of immunological tolerance in oral cancer, Presenting a new concept oral cancer prevention and treatment strategy through identification of major molecular targets and mechanisms related to oral cancer development, 구강암 발병관련 주요 분자표적 및 기전 규명을 통한 신개념 구강암 예방 및 치료전략 제시, 구강암 전이관련 분자표적 발굴 및 신호전달체계 규명, 구강암에서 면연관용의 역할 규명

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