| Project/Area Number |
25462504
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Urology
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| Research Institution | Japanese Foundation for Cancer Research |
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Principal Investigator |
Takeshi Yuasa 公益財団法人がん研究会, その他部局等, 研究員 (00314162)
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| Co-Investigator(Renkei-kenkyūsha) |
Takahiro Isono 滋賀医科大学, 実験実習支援センター, 准教授 (20176259)
Yuichi Ishikawa (公財)がん研究会, がん研究所病理センター, センター長 (80222975)
Yonese Junji (公財)がん研究会有明病院, 泌尿器科, 部長 (70469633)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 腎癌 / 分子標的治療 / 次世代シーケンサー / 遺伝子発現 / 糖枯渇 / 腎がん / 治療耐性 / VHL遺伝子 / 腎細胞がん / 血管新生阻害剤 / グルコース枯渇 / 小胞体ストレス |
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| Outline of Final Research Achievements |
Resistance to the targeted therapy is emerging as an obstacle to successful cancer treatment. In this study, we investigated whether N-GlcNAc2-modified proteins induce G2/M arrest and cell death under glucose deprivation in renal cell cancer (RCC), which is sensitive to nutritional stress. Four of seven RCC cell lines produced N-GlcNAc2-modified proteins and led G2/M arrest under glucose deprivation, leading to cell death. The remaining three cell lines did not produce N-GlcNAc2-modified proteins and undergo G1/S arrest, leading to survival. In this study, we demonstrated that the RCC cells which accumulate N-GlcNAc2-modified proteins do not survive with abnormally prolonged unfolded protein response (UPR) pathway. By contrast, cells that do not accumulate N-GlcNAc2-modified proteins survive. Further studies to clarify these findings will lead to the development of novel targeted therapy for RCC.
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