Identification of the mechanisms of metabolic stress signal for the treatment of oral cancer
| Project/Area Number |
15H05019
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Pathobiological dentistry/Dental radiology
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| Research Institution | University of Miyazaki |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
高雄 啓三 富山大学, 研究推進機構 研究推進総合支援センター, 教授 (80420397)
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| Co-Investigator(Renkei-kenkyūsha) |
KATO Hironori 宮崎大学, 医学部, 特任助教 (40610283)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥17,160,000 (Direct Cost: ¥13,200,000、Indirect Cost: ¥3,960,000)
Fiscal Year 2017: ¥5,850,000 (Direct Cost: ¥4,500,000、Indirect Cost: ¥1,350,000)
Fiscal Year 2016: ¥5,850,000 (Direct Cost: ¥4,500,000、Indirect Cost: ¥1,350,000)
Fiscal Year 2015: ¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
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| Keywords | 小胞体ストレス / 蛋白質 / ストレス応答 |
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| Outline of Final Research Achievements |
Cancers that occur frequently in the oral cavity are in a state of low oxygen / low glucose stress because there is not sufficient angiogenesis, and the cancer cells are in a very high metabolic requirement. Under such stress, autophagy is thought to contribute to cell proliferation. In addition, malnutrition leads to accumulation of bad proteins and ER stress-induced survival / proliferation signals are transmitted. One way to overcome oral cancers in a stress tolerant state is to suppress the survival signal transmitted from autophagy or the endoplasmic reticulum and to induce a cell death signal due to strong endoplasmic reticulum stress. In this study, the metabolic stress signal in cancer cells was elucidated.
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Report
(4 results)
Research Products
(13 results)
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[Journal Article] A mouse model reveals that Mfsd2a is critical for unfolded protein response upon exposure to tunicamycin.2017
Author(s)
Moritake H, Obara M, Saito Y, Kashimada A, Takagi M, Funakoshi-Tago M, Fukuyama T, Yoshioka M, Inoue A, Komatsu H, Nishitoh H, Kataoka H, Nunoi H.
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Journal Title
Hum Cell.
Volume: 30
Issue: 2
Pages: 88-97
DOI
Related Report
Peer Reviewed
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[Journal Article] A systematic immunoprecipitation approach reinforces the concept of common conformational alterations in amyotrophic lateral sclerosis-linked SOD1 mutants.2015
Author(s)
Fujisawa, T., Yamaguchi, N., Kadowaki, H., Tsukamoto, Y., Tsuburaya, N., Tsubota, A., Takahashi, H., Naguro, I., Takahashi, Y., Goto, J., Tsuji, S., Nishitoh, H., Homma, K. and Ichijo, H.
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Journal Title
Neurobiol. Dis.
Volume: 82
Issue: 2
Pages: 478-486
DOI
Related Report
Peer Reviewed / Open Access / Int'l Joint Research / Acknowledgement Compliant
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