| Project/Area Number |
24701032
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Clinical oncology
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| Research Institution | Iwate Medical University |
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Principal Investigator |
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
|
| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | GATA-6 / 転写因子 / 大腸癌 / PKA / JNK / cancer / cAMP |
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| Research Abstract |
GATA-6 is transcription factor essential for differentiation or proliferation of early embryonic cells. Recently it is reported that GATA-6 involved proliferation and surviving of gastrointestinal tumor cells. In this study, I configured the research theme, "How effective is the degradation of GATA-6 as novel molecular target of chemotherapy for colorectal cancer". Especially I focused on two issues, (1) Identification of signal transduction pathway for degradation of GATA-6, and (2) Estimation of effectiveness of degradation of GATA-6 as novel anti-tumor chemotherapy. Experiment for (1) resulted that novel kinase pathway activating JNK involved degradation of GATA-6 via nuclear export pathway. The other experiment for (2) showed that JNK activator inducing proteolysis of GATA-6 arrested the cell cycle at G2/M phase, and suppressed proliferation of colorectal cancer cells.
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