Anti-tumor effects by recombinant STAT3-inhibiting Sendai virus
| Project/Area Number |
15K15143
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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 |
Virology
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| Research Institution | Hiroshima University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
IRIE TAKASHI 広島大学, 大学院医歯薬保健学研究院, 准教授 (70419498)
FUKUSHI MASAYA 広島大学, 大学院医歯薬保健学研究院, 助教 (50313515)
ODA KOSUKE 広島大学, 大学院医歯保健学研究院, 助教 (60571255)
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2016: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | STAT3 / センダイウイルス / Ｃ蛋白質 / アクセサリー蛋白質 / 抗腫瘍効果 / 癌治療 / シグナル伝達機構 / C蛋白質 / シグナル伝達 |
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| Outline of Final Research Achievements |
Our purpose is that we generate a recombinant Sendai virus expression the STAT3-interacting C protein to cause apoptosis in tumor cells for cancer gene therapy. We recently determined crystal structure of the complex of the C protein and STAT1. Based on the detailed information of interacting surface, we predicted amino acid mutations that cause binding of the C protein and STAT3, which is closely related to STAT1. However, we could not obtain the STAT3-interacting C protein after several attempts by the collaboration with a crystallographer and a theoretical biologist by the end of research period. The original wild-type C protein seemed to inhibit the STAT3 activation probably through the inhibition of STAT1, but this did not bring sufficient inhibition of STAT3. It is necessary for us to proceed “wet” experiments including phage display, not in silico protein structure prediction.
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Report
(3 results)
Research Products
(5 results)
