| Project/Area Number |
22791243
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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 |
General surgery
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| Research Institution | Hirosaki University |
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Principal Investigator |
MOROHASHI Satoko 弘前大学, 医学(系)研究科(研究院), 助教 (90569592)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
Fiscal Year 2012: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2011: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2010: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
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| Keywords | 時計遺伝子 / 乳癌 / 治療 / アポトーシス / DEC / 転写因子 |
|---|
| Research Abstract |
Expression of clock genes, DEC1 and DEC2 were up-regulated in the MCF-7 human breast cancer cells by TNF-α in a concentration-dependent manner. TNF-α induced the apoptosis of MCF-7 cells. We also demonstrated that siRNA-mediated DEC2 knockdown, but not DEC1, increased the Bax expression, cleavage PARP and cleavage caspase-7 in MCF-7 cells. In conclusion, we speculated that DEC2 plays an important role in the regulation of both apoptosis and proliferation of the MCF-7 cells.
In human breast cancer MCF-7 cells, paclitaxel increased the expression of DEC1 and DEC2. However, DEC1 and DEC2 exhibited opposite effects in paclitaxel inducing apoptosis, That is DEC1 has pro-apoptotic, while DEC2 has anti-apoptotic function. Both the two transcription factors play important roles in regulating paclitaxel induced apoptosispathway.
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