| Project/Area Number |
23501313
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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 |
Clinical oncology
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| Research Institution | Nihon University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
FUKUDA Noboru 日本大学, 総合科学研究科, 教授 (40267050)
UENO Takahiro 日本大学, 医学部, 准教授 (40386008)
FUJIWARA Kyoko 日本大学, 医学部, 助教 (40595708)
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| Co-Investigator(Renkei-kenkyūsha) |
NAGASE Hiroki 千葉県がんセンター, 研究局, 研究所長 (90322073)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2013: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2012: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
Fiscal Year 2011: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
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| Keywords | ピロール・イミダゾール・ポリアミド / E-box / MYC / 抗腫瘍効果 / Myc / 抗腫瘍薬 / ポリアミド / がん / E-box配列 |
|---|
| Research Abstract |
Gene amplification and/or overexpression of the transcription factor c-MYC, which binds to E-box (5'-CACGTG-3') present within its numerous target gene promoters, has been observed in many human tumors. In this study, we have designed pyrrole-midazole polyamides (PIP), which could bind to E-box, and investigated their possible effects on human cancer cells. We found that some PIP we designed significantly suppressed growth of osteosarcoma cell MG63 and leukemia cell K562. According to our present results, PIP-treated cells underwent apoptosis and/or G1 arrest. Furthermore, intravenous injection of PIP markedly repressed MG63-derived tumor development in nude mice. Intriguingly, knockdown of the putative PIP target MALAT1 encoding long non-coding RNA remarkably impaired cell growth of MG63 cells. Collectively, our present findings strongly suggest that PIP exerts its tumor-suppressive ability at least in part through the specific down-regulation of MALAT1.
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