The role of glucocorticoid in mitochondria-dependent resistance to anticancer therapy
| Project/Area Number |
24501353
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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 |
Clinical oncology
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| Research Institution | Osaka City University |
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Principal Investigator |
KASAHARA EMIKO 大阪市立大学, 医学(系)研究科(研究院), 講師 (30468269)
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| Co-Investigator(Kenkyū-buntansha) |
KUBO Shuji 兵庫医科大学, 医学部, 准教授 (10441320)
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| Co-Investigator(Renkei-kenkyūsha) |
SEKIYAMA Atsuo 大阪大学, 薬学研究科, 教授 (30403702)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2012: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | グルココルチコイド / ミトコンドリア / 抗がん剤 / ストレス / 中皮腫 / シスプラチン / 薬剤耐性 / 抗がん剤耐性 |
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| Outline of Final Research Achievements |
Those intense stress by a side effect of chemotherapy as well as the pain with the cancer also influence the therapeutic effects of the anticancer agents.
However, little is known about the mechanisms of these untoward actions. In this study, we investigated the influence of glucocorticoids, which is a stress-related hormone on anticancer drug actions. Our results suggest that stress-induced glucocorticoids attenuate the action of anticancer drug through the alteration of mitochondrial function.
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Report
(4 results)
Research Products
(13 results)
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[Journal Article] Stress-Induced Glucocorticoid Release Upregulates Uncoupling Protein-2 Expression and Enhances Resistance to Endotoxin-Induced Lethality2015
Author(s)
Kasahara E, Sekiyama A, Hori M, Kuratsune D, Fujisawa N, Chida D, Hiramoto H, Li J, Okamura H, Inoue M, Kitagawa S.
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Journal Title
Neuroimmunomodulation
Volume: ー
Issue: 5
Pages: 279-292
DOI
Related Report
Peer Reviewed / Acknowledgement Compliant
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[Journal Article] Haploinsufficiency of the c-myc transcriptional repressor FIR, as a dominant negative-alternative splicing model, promoted p53-dependent T-cell acute lymphoblastic leukemia progression by activating Notch1.2015
Author(s)
Matsushita K, Kitamura K, Rahmutulla B, Tanaka N, Ishige T, Satoh M, Hoshino T, Miyagi S, Mori T, Itoga S, Shimada H, Tomonaga T, Kito M, Nakajima-Takagi Y, Kubo S, Nakaseko C, Hatano M, Miki T, Matsuo M, Fukuyo M, Kaneda A, Iwama A, Nomura F.
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Journal Title
Oncotarget
Volume: 10
Pages: 5102-17
Related Report
Peer Reviewed
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[Journal Article] Alternative splicing of FBP-interacting repressor coordinates c-Myc, P27Kip1/ cyclinE and Ku86/ XRCC5 expression as a molecular sensor for bleomycin-induced DNA damage pathway.2014
Author(s)
Rahmutulla B, Matsushita K, Satoh M, Seimiya M, Tsuchida S, Kubo S, Shimada H, Ohtsuka M, Miyazaki M, Nomura F.
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Journal Title
Oncotarget
Volume: 15
Pages: 2404-17
Related Report
Peer Reviewed
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