2016 Fiscal Year Final Research Report
Mechanism of multidrug resistance caused after the treatment targeting CD44, and the strategy for overcoming the resistance in head and neck squamous cell carcinoma.
| Project/Area Number |
26462854
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Pathobiological dentistry/Dental radiology
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| Research Institution | Aomori University (2015-2016)
Meikai University (2014) |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
TOMOMURA Mineko 明海大学, 総合教育セ, 教授 (30217559)
SUGIMOTO Masahiro 慶應義塾大学, 先端生命科学研, 教授 (30458963)
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| Research Collaborator |
GOTO Masuo University of North Carolina at Chapel Hill, Pharmacy Research Assistant Professor
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Keywords | 薬剤耐性 / がん幹細胞 |
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| Outline of Final Research Achievements |
Many studies have demonstrated that a variety of human malignancies, including head and neck squamous cell carcinoma (HNSCC), contain subpopulations of cells called cancer stem-like cells (CSCs) that exhibit stem cell-like properties, such as self-renewal and tumor-initiating capabilities. CD44 is a marker of cancer stem cells in HNSCC, and CD44 expression is related to prognosis in cancer patients. The resistance of CSCs to conventional chemoradiotherapy may involve enhanced DNA damage repair pathways and alterations in cell cycle kinetics. Chk1 mediates S and G2 arrests. Our findings suggest that CD44 plays a role in enhancing the DNA damage response coordinated by Chk1. As part of a study of acquired multidrug resistance, then HSC-3 was grown in gradually increasing cisplatin concentrations and selected a resistant subline denote R HSC-3. R HSC-3 showed cross-resistance to several anticancer agents. The multidrug transporter, ABCG2, and CD44 were upregulated in R HSC-3 cells.
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| Free Research Field |
歯科薬理学
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