Clarifying the significance of the shift to aerobic glycolysis and the role of mitochondrial function in kidney cancer development
| Project/Area Number |
15K14370
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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 |
Laboratory animal science
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| Research Institution | Kumamoto University |
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Principal Investigator |
Baba Masaya 熊本大学, 国際先端医学研究機構, 准教授 (10347304)
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| Co-Investigator(Renkei-kenkyūsha) |
SETOU MITSUTOSHI 浜松医科大学, 医学部, 教授 (20302664)
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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 |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 腎細胞癌 / 糖代謝 / ミトコンドリア / マウスモデル / 腎がん / 疾患モデル |
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| Outline of Final Research Achievements |
Aerobic glycolysis predominates over mitochondrial oxidative phosphorylation in cancer. Cancer cells utilize this metabolic shift to aerobic glycolysis to drive proliferation and progression. However, the significance of this metabolic shift and the role of mitochondrial function during cancer development remains to be determined. Previously, we reported that mitochondrial biogenesis was upregulated with increased transcriptional activity of TFE3 in a rare type of hereditary renal cell carcinoma (RCC). This research aims to clarify the significance of the shift to aerobic glycolysis and the role of mitochondrial function in TFE3 translocation RCC, in which TFE3 transcriptional activity is constitutively activated by translocation. We have generated and analyzed a variety of TFE3-inducible stable cell lines and a mouse model of TFE3 translocation RCC, and found a potential function of ATP produced in the mitochondria as a signaling molecule which may contribute to cancer development.
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Report
(3 results)
Research Products
(35 results)
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[Journal Article] Establishment and characterization of BHD-F59RSVT, an immortalized cell line derived from a renal cell carcinoma in a patient with Birt-Hogg-Dube syndrome2017
Author(s)
Furuya M, Hasumi H, Baba M, Tanaka R, Iribe Y, Onishi T, Nagashima Y, Nakatani Y, Isono Y, Yao M.
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Journal Title
Laboratory Investigation
Volume: 97
Issue: 3
Pages: 343-351
DOI
Related Report
Peer Reviewed / Open Access / Acknowledgement Compliant
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[Journal Article] H255Y and K508R missense mutations in tumour suppressor folliculin (FLCN) promote kidney cell proliferation.2017
Author(s)
Hasumi H, Hasumi Y, Baba M, Nishi H, Furuya M, Vocke CD, Lang M, Irie N, Esumi C, Merino MJ, Kawahara T, Isono Y, Makiyama K, Warner AC, Haines DC, Wei MH, Zbar B, Hagenau H, Feigenbaum L, Kondo K, Nakaigawa N, Yao M, Metwalli AR, Marston Linehan W, Schmidt LS
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Journal Title
Human Molecular Genetics
Volume: 26
Pages: 354-366
DOI
Related Report
Peer Reviewed / Open Access / Int'l Joint Research / Acknowledgement Compliant
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[Journal Article] Genetic, epidemiologic and clinicopathologic studies of Japanese Asian patients with Birt-Hogg-Dube syndrome.2016
Author(s)
Furuya M, Yao M, Tanaka R, Nagashima Y, Kuroda N, Hasumi H, Baba M, Matsushima J, Nomura F, Nakatani Y
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Journal Title
Clinical Genetics
Volume: 90
Issue: 5
Pages: 403-412
DOI
Related Report
Peer Reviewed / Open Access / Acknowledgement Compliant
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[Journal Article] Loss of Folliculin Disrupts Hematopoietic Stem Cell Quiescence and Homeostasis Resulting in Bone Marrow Failure2016
Author(s)
Baba M, Toyama H, Sun L, Takubo K, Suh HC, Hasumi H, Nakamura-Ishizu A, Hasumi Y, Klarmann KD, Nakagata N, Schmidt LS, Linehan WM, Suda T, Keller JR
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Journal Title
Stem Cells
Volume: 34
Issue: 4
Pages: 1068-1082
DOI
Related Report
Peer Reviewed / Open Access / Int'l Joint Research / Acknowledgement Compliant
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