| Project/Area Number |
24592588
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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 |
Otorhinolaryngology
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| Research Institution | Yokohama City University |
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Principal Investigator |
ORIDATE Nobuhiko 横浜市立大学, 医学(系)研究科(研究院), 教授 (90312355)
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| Co-Investigator(Kenkyū-buntansha) |
NASHIMOTO Masayuki 新潟薬科大学, 応用生物科学部, 教授 (30228069)
TAMURA Masato 北海道大学, 歯学研究科(研究院), 教授 (30236757)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2014: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2012: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | 頭頸部癌 / TRUE gene silencing / 頭頸部癌治療 / small guide RNA / heptamer型 sgRNA / 低侵襲 / 化学療法併用放射線治療 / heptamer型sgRNA / TRUE gene silencing法 / RNA干渉 / cyclinD1 / 頭頸部癌細胞 / サイクリンＤ１ / 遺伝子発現抑制法 / tRNase ZL |
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| Outline of Final Research Achievements |
Head and neck squamous cell carcinoma (HNSCC) exhibits increased expression of cyclin D1. Previous studies have shown a correlation between poor prognosis of HNSCC and cyclin D1 overexpression. tRNase ZL-utilizing efficacious gene silencing (TRUE gene silencing) is one of the RNA-mediated gene expression control technologies that have therapeutic potential. This technology is based on a unique enzymatic property of mammalian tRNase ZL, which is that it can cleave any target RNA at any desired site by recognizing a pre-tRNA-like complex formed between the target RNA and an artificial small guide RNA (sgRNA). In this study, we designed several sgRNAs targeting human cyclin D1 mRNA to examine growth inhibition of HNSCC cells. Transfection of certain sgRNAs decreased levels of cyclin D1 mRNA and protein in HSC-2 and HSC-3 cells, and also inhibited their proliferation. The combination of these sgRNAs and cisplatin showed more than additive inhibition of cancer cell growth.
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