| Project/Area Number |
25293082
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Partial Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Pathological medical chemistry
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| Research Institution | Saitama Medical University |
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Principal Investigator |
Okuda Akihiko 埼玉医科大学, 医学部, 教授 (60201993)
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| Co-Investigator(Kenkyū-buntansha) |
KATO HIDEMASA 埼玉医科大学, 医学部, 講師 (50292123)
HIRASAKI MASATAKA 埼玉医科大学, 医学部, 助教 (10522154)
EMA MASATSUGU 滋賀医科大学, 動物生命科学研究センター, 教授 (60359578)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥17,420,000 (Direct Cost: ¥13,400,000、Indirect Cost: ¥4,020,000)
Fiscal Year 2015: ¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2014: ¥5,850,000 (Direct Cost: ¥4,500,000、Indirect Cost: ¥1,350,000)
Fiscal Year 2013: ¥7,410,000 (Direct Cost: ¥5,700,000、Indirect Cost: ¥1,710,000)
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| Keywords | ES細胞 / がん細胞 / 細胞増殖 / アポトーシス / c-Myc / Nucleostemin / Max / 癌細胞 |
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| Outline of Final Research Achievements |
In this study, we explored the molecular bases defining the similarities between ES cells and cancer cells through the analyses of Myc and nucleostemin which are both known as important regulators in both cell types. First, we demonstrated that apoptotic phenotype of nucleostemin-null ES cells was erased by the forced expression of Nanog or Esrrb. As to the Myc studies, we demonstrated that apoptotic phenotype overexpressed with Myc in normal somatic cells reflect the intrinsic activity of Myc free from Max association which becomes evident because the amount of Myc protein exceeds much more than that of the endogenous Max due the forced expression. Furthermore, our data demonstrated that ES cells and cancer cells, but not normal somatic cells, bear proteins which suppress the intrinsic apoptotic inducing activity of Myc which is liberated from the regulation by Max.
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