| Project/Area Number |
22790347
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Human pathology
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| Research Institution | Iwate Medical University |
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Principal Investigator |
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| Project Period (FY) |
2010 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
|
| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2011: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2010: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 分子病理 / 脳腫瘍 / β-TrCP / 悪性度 / 神経幹細胞 / 分化異常 |
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| Research Abstract |
(1) The expression ofβIII-tubulin is generally restricted to neurons, but its mRNA is often expressed at a low level in non-neuronal cells. Here, we present evidence thatβIII-tubulin expression occurs in a cell cycle-dependent manner. Both mRNA and protein ofβIII-tubulin accumulated around the G2/M stage of the cell cycle. Furthermore, the cell cycle-dependent expression ofβIII-tubulin was mediated by the neural-restrictive silencing factor NRSF/REST through its binding to the NRSE/RE-1 element that is present in the first intron of theβIII-tubulin gene. These results demonstrate a novel role ofβIII-tubulin in cell cycle progression in tumor cells.
(2) Post-transcriptional acetylation-modification of cortactin(CTTN) via the nucleus accumbens-associated 1(NACC1)-histone deacetylase 6(HDAC6) deacetylation system were investigated. The acetylation status of CTTN modulated by the NACC1-HDAC6 deacetylation system induces acceleration of cell migration activity via an actin-dependent cellular process, possibly contributing to aggressive behavior(invasion/metastasis) of the tumor cells.
(3) MicroRNAs(miRNAs) are small non-coding RNAs whose aberrations are involved in the initiation and progression of human cancers. We focused on one commonly downregulated miRNA(miR-211), and analyzed its relationship to the expression of preferentially expressed antigen of melanoma(PRAME) protein, which is a potential target of miR-211.These results suggest that downregulation of miR-211 may be partly involved in aberrant expression of the PRAME protein in melanoma cells.
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