2017 Fiscal Year Final Research Report
Does NANOG have the potential to regulate immune escape of cancer stem cells?
| Project/Area Number |
16K15236
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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 |
Pathological medical chemistry
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| Research Institution | Osaka University |
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Principal Investigator |
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Keywords | 癌幹細胞 / Nanog / NK細胞 |
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| Outline of Final Research Achievements |
In cancer stem-like cells, high expression of Nanog and low expression of ICAM-1 were discovered. Nanog expression inhibited ICAM-1 expression in cancer cells, which suppressed the sensitivity of cancer cells to NK cells. Xenograft experiments were performed in SCID mice using cancer cells with Nanog-overexpression or Nanog suppression by Nanog shRNA. It was concluded that Nanog expression accelerated tumor growth in mice by lowering NK cell sensitivity through the suppression of ICAM-1. ChIP seq analysis revealed that Nanog bound to the ICAM-1 promoter sited and inhibited the association of histone acetylase p300 with ICAM-1 promoter. Clinical sample analysis demonstrated the inverse correlation of Nanog and ICAM-1 expression.
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| Free Research Field |
遺伝子治療学
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