Analysis of the gene transcriptional network system regulated by nuclear tumor suppressive factors
| Project/Area Number |
17054039
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| Research Category |
Grant-in-Aid for Scientific Research on Priority Areas
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| Allocation Type | Single-year Grants |
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| Review Section |
Biological Sciences
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| Research Institution | Nippon Medical School |
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Principal Investigator |
TANAKA Nobuyuki Nippon Medical School, 大学院・医学研究科, 教授 (80222115)
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| Co-Investigator(Kenkyū-buntansha) |
ABE Yoshinori 日本医科大学, 老人病研究所, 助教 (00386153)
UEHARA Ikuno 日本医科大学, 老人病研究所, 助教 (50434139)
NAKAJIMA Wataru 日本医科大学, 老人病研究所, 助教 (40557500)
SATO Eri 日本医科大学, 老人病研究所, 講師 (90339440)
KAWAUTI Keiko 日本医科大学, 老人病研究所, 講師 (40434138)
TOBIUME Kei 日本医科大学, 老人病研究所, 講師 (40350037)
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| Project Period (FY) |
2005 – 2009
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| Project Status |
Completed (Fiscal Year 2009)
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| Budget Amount *help |
¥86,000,000 (Direct Cost: ¥86,000,000)
Fiscal Year 2009: ¥12,600,000 (Direct Cost: ¥12,600,000)
Fiscal Year 2008: ¥12,600,000 (Direct Cost: ¥12,600,000)
Fiscal Year 2007: ¥19,600,000 (Direct Cost: ¥19,600,000)
Fiscal Year 2006: ¥19,600,000 (Direct Cost: ¥19,600,000)
Fiscal Year 2005: ¥21,600,000 (Direct Cost: ¥21,600,000)
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| Keywords | 癌化 / 癌抑制 / p53 / グルコース代謝 / NF-κB / グルコーストランスポーター / O-GlcNAc修飾 / P53 / 発癌 / IL-6 / Stat3 / Hedeho sinal / Mdm2 / NF-KB / IKKα / B / Hedgehog signal / β / 足場非依存性増殖 / 癌遺伝子 / GLUT3 / Aurora-A / 細胞周期制御 / Hedgehogシグナル |
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| Research Abstract |
Cancer cells preferentially utilize aerobic glycolysis for energy provision and this metabolic change is important for tumour growth. In this study period, we found that tumor suppressor p53 limits glycolysis. and that loss of function of p53 induces enhancement of glycolysis through activation of the treansciption factor NF-κB. We also found that enhanced glycolysis is essential for oncogene-induced cell transformation in p53-deficient cells, and propose a novel mechanism for tumor suppression by p53.
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Report
(6 results)
Research Products
(59 results)
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[Journal Article] Interleukin 6 enhances glycolysis through expression of the glycolytic enzymes hexokinase2and6-phosphofructo-2-kinase/fructose-2, 6-bisphosphatase-3.2010
Author(s)
Ando, M., Uehara, I., Kogure, K., Asano, Y., Nakajima, W., Abe, Y., Kawauchi, K., Tanaka, N.
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Journal Title
J Nippon Med Sch 77
Pages: 97-105
Related Report
Peer Reviewed
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[Journal Article] Critical role for constitutive type I interferon signaling in the prevention of cellular transformation.2009
Author(s)
Chen, H.M., Tanaka, N., Mitani, Y., Oda, E., Nozawa, H., Chen, J.Z., Yanai, H., Negishi, H., Choi, M.K., Iwasaki, T., et al.
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Journal Title
Cancer Sci 100
Pages: 449-456
NAID
Related Report
Peer Reviewed
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[Journal Article] Hedgehog signaling overrides p53-mediated tumor suppression by activating Mdm2.2008
Author(s)
Abe, Y., Oda-Sato, E., Tobiume, K., Kawauchi, K., Taya, Y., Okamoto, K., Oren, M., Tanaka, N.
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Journal Title
Proc Natl Acad Sci U S A 105
Pages: 4838-4843
Related Report
Peer Reviewed
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[Journal Article] 5-Aza-2'-deoxycytidine restores proapoptotic function of p53 in cancer cells resistant to p53-induced apoptosis.2008
Author(s)
Yagi, S., Oda-Sato, E., Uehara, I., Asano, Y., Nakajima, W., Takeshita, T., Tanaka, N.
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Journal Title
Cancer Invest 26
Pages: 680-688
Related Report
Peer Reviewed
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[Presentation] Negatve regulation of p53 by Hedgehog signaling.2007
Author(s)
Abe, Y., Oda-Sato, E., Tobiume, K., Kawauchi, K., Tanaka, N.
Organizer
EMBO WORKSHOP 2007, Molecular Mechanisms of Cell Cycle Control in Normal & Malignant Cells
Place of Presentation
Spetses Island, Greece
Related Report
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