| Project/Area Number |
15K10921
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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 |
Pediatric surgery
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| Research Institution | Hiroshima University |
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Principal Investigator |
YAMAOKA EMI 広島大学, 自然科学研究支援開発センター, 研究員 (20403503)
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| Co-Investigator(Kenkyū-buntansha) |
栗原 將 広島大学, 医歯薬保健学研究科(医), 助教 (40724894)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 小児がん / 神経芽腫 / 予後因子 / Neuroblasoma |
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| Outline of Final Research Achievements |
We performed functional analysis of DHRS3, CYP26A1 and NR0B1, highly expressed in favorable neuroblastoma transfected into neuroblastoma cell lines such as SKNSH, NH12, TGW, GOTO and NH6 with an overexpression and silensing system. DHRS3 and NR0B1 induced cell proliferation, cell cycle suppression, decreased tumorigenic ability.
In exhaustive transcriptome analysis using RNAseq, expression of genes related to cell cycle and cell proliferation was decreased. We found the group of genes involved in the suppression of TGF-βsignaling involved in the retinoid X receptor activation pathway, JNKsignaling, tumor suppression and promotion of tumor growth. Therefore, DHRS3 and NR0B1 may be associated with spontaneous degeneration of neuroblastoma.
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