| Project/Area Number |
20591575
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Digestive surgery
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| Research Institution | Wakayama Medical University |
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Principal Investigator |
UEDA Kentaro Wakayama Medical University, 医学部, 助教 (20438279)
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| Co-Investigator(Kenkyū-buntansha) |
YAMAUE Hiroki 和歌山県立医科大学, 医学部, 教授 (20191190)
IWAHASHI Makoto 和歌山県立医科大学, 医学部, 講師 (70244738)
NAKAMORI Mikihito 和歌山県立医科大学, 医学部, 講師 (10322372)
NAKAMURA MASAKI 和歌山県立医科大学, 医学部, 助教 (80364090)
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| Project Period (FY) |
2008 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
Fiscal Year 2010: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2009: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2008: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | NPRL2遺伝子 / 食道癌 / 放射線治療 / 遺伝子 / 癌 / 放射線科 / 放射線 |
|---|
| Research Abstract |
In 10 human esophageal cancer cell lines, the IC50 of radiation ranged from IC50 1.58Gy to 9.28Gy. There were no expression of NPRL2 protein in these cell lines, on the other hand, Rad51 protein showed strong expression in all cell lines. The levels of NPRL2 or Rad51 expression did not correlate with radiosensitivity. Tumor growth inhibition rate of NPRL2 vector was about 30% for human esophageal cancer cells, and combination therapy of NPRL2 vector and IC20 of radiation therapy enhanced this inhibitory effect to around 60 percent. We prepared some Rad51-siRNA vectors, however, these Rad51-siRNA vector did not inhibit expression of Rad51 protein. To investigate the mechanism of combined effect of NPRL2 vector, we made four groups ; 1) control group, 2) radiation therapy (IC20), 3) NPRL2 group, 4) NPRL2+radiotherapy. NPRL2+radiation therapy groupactivated DNA damage pathway, and showed a strong G2 arrest and apoptosis, compared with the other group.
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