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KAKEN_23590134seika.pdf
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Download
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:182.5 KB
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| Last updated |
:Dec 11, 2014 |
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Total downloads since Dec 11, 2014 : 1742
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| Title |
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がんウイルスEpstein-Barr Virusに対する新規分子標的薬の開発
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ガン ウイルス Epstein-Barr Virus ニ タイスル シンキ ブンシ ヒョウテキヤク ノ カイハツ
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Gan uirusu Epstein-Barr Virus ni taisuru shinki bunshi hyotekiyaku no kaihatsu
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Development of molecular target therapy for EBV
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野口, 耕司
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ノグチ, コウジ
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Noguchi, Koji
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慶應義塾大学•薬学部・准教授
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Research team head
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科研費研究者番号 : 80291136
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2014
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科学研究費補助金研究成果報告書
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2013
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我々は、ヒトがんウイルスEpstein-Barr virus/EBVに対する新規分子標的薬の開発を目指している。本研究課題では、DNAに結合するピロールイミダゾールポリアミド化合物に着目し、EBV発がんに重要なEBNA1蛋白質のDNA結合を抑制する抗EBNA1阻害剤の開発を試みた。その結果、一つのポリアミド化合物に、EBNA1-DNA結合の阻害活性が認められた。このポリアミド化合物は、EBV感染による正常B細胞の形質転換を顕著に抑制することが示された。これらの結果、EBV感染がんに対する新規の分子標的薬としてEBNA1阻害化合物が有望である事が明らかになった。
Epstein-Barr Virus (EBV) transforms human B lymphocytes into immortalized cells in vitro, and is associated with various malignancies in vivo. DNA-binding protein EBNA1 plays critical role for the viral episome maintenance and transactivates viral transforming genes in latently infected cells. Therefore, DNA-targeting agents that can disrupt the EBNA1-DNA interaction will offer novel functional inhibitors of EBNA1. Here, a synthetic pyrrole-imidazole polyamide bound adjacent to the EBNA1 recognition sequences located in the dyad symmetry element of oriP, and selectively inhibited EBNA1-oriP binding. This polyamide inhibited EBV-mediated B-cell immortalization. These results suggest that EBNA1 functions will be an attractive pharmacological target for EBV-associated diseases.
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研究種目 : 基盤研究(C)
研究期間 : 2011～2013
課題番号 : 23590134
研究分野 : 医歯薬学
科研費の分科・細目 : 薬学・創薬化学
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