Epigenetic abnormality induced by aberrant c-Myc expression leads to the chromosomal instability.
| Project/Area Number |
26670668
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Orthopaedic surgery
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| Research Institution | Oita University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
TANAKA Kazuhiro 大分大学, 医学部人工関節講座, 講師 (10274458)
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 肉腫 / 染色体不安定性 / ｃ－ｍｙｃ / 染色体転座 / エピジェネティクス / cmyc |
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| Outline of Final Research Achievements |
By forcing c-Myc expression and performing ChIP-sequence in that state, we have analyzed and verified data by microRNA and cDNA array. Currently it is likely that let-7a, miR-16, miR-29b, miR-1294, and/or miR-2682 are involved. We demonstrated that the transfection of these two factors suppresses the expression of mRNA and protein on c-Myc, and also suppresses the progression of the cell cycle.To examine the presence or absence of chromosomal instability during the study period, we are attempting to detect abnormalities in genome fraction and in the number of DNA copies using the DNA ploidy analysis and array-CGH. Our prediction is that one of the DSB repair systems, homologous recombination or non-homologous end joining, has a greater dysfunction. We are seeking to determine this through HR activity measurement in c-myc-introduced fibroblasts by I-Scel, and random plasmid integration, which is an NHEJ assay.
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Report
(3 results)
Research Products
(12 results)
