Study on the mechanisms of tumor progression induced by dysregulation of Src oncoprotein
Project/Area Number |
15H04296
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Research Category |
Grant-in-Aid for Scientific Research (B)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Tumor biology
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Research Institution | Osaka University |
Principal Investigator |
Okada Masato 大阪大学, 微生物病研究所, 教授 (10177058)
|
Co-Investigator(Kenkyū-buntansha) |
小根山 千歳 愛知県がんセンター(研究所), 感染腫瘍学部, 部長 (90373208)
|
Project Period (FY) |
2015-04-01 – 2018-03-31
|
Project Status |
Completed (Fiscal Year 2017)
|
Budget Amount *help |
¥16,900,000 (Direct Cost: ¥13,000,000、Indirect Cost: ¥3,900,000)
Fiscal Year 2017: ¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2016: ¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2015: ¥7,280,000 (Direct Cost: ¥5,600,000、Indirect Cost: ¥1,680,000)
|
Keywords | がん進展 / 浸潤転移 / Src / チロシンキナーゼ / がん遺伝子 / 腫瘍進展 / 上皮間葉転換 / TGFβ / 癌 / シグナル伝達 / 浸潤・転移 / 発現制御 |
Outline of Final Research Achievements |
Src tyrosine kinase is the first-identified onco-protein, and plays a crucial role in promoting tumor malignancy, such as invasive and metastatic ability, when its function is upregulated during tumor progression. However, molecular mechanism underlying the dysregulation of Src expression/activity and its actual roles in tumor progression remain elusive. To address these issues, we analyzed the regulatory mechanism of SRC gene expression and the functions of scaffold proteins that activate Src. Based on these analyses, we proposed new models of the molecular mechanisms for Src-mediated tumor progression.
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Report
(4 results)
Research Products
(27 results)
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[Journal Article] Structural basis for the assembly of the Ragulator-Rag GTPase complex.2017
Author(s)
Yonehara R, Nada S, Nakai T, Nakai M, Kitamura A, Ogawa A, Nakatsumi H, Nakayama KI, Li S, Standley DM, Yamashita E, Nakagawa A, Okada M.
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Journal Title
Nat Commun.
Volume: 8
Issue: 1
Pages: 1625-1625
DOI
Related Report
Peer Reviewed / Open Access / Int'l Joint Research
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[Journal Article] Lamtor1 Is Critically Required for CD4+ T Cell Proliferation and Regulatory T Cell Suppressive Function.2017
Author(s)
Hosokawa T, Kimura T, Nada S, Okuno T, Ito D, Kang S, Nojima S, Yamashita K, Nakatani T, Hayama Y, Kato Y, Kinehara Y, Nishide M, Mikami N, Koyama S, Takamatsu H, Okuzaki D, Ohkura N, Sakaguchi S, Okada M, Kumanogoh A.
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Journal Title
J Immunol.
Volume: 199
Issue: 6
Pages: 2008-2019
DOI
Related Report
Peer Reviewed / Open Access
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[Journal Article] The Rho guanine nucleotide exchange factor ARHGEF5 promotes tumor malignancy via epithelial-mesenchymal transition2016
Author(s)
Komiya Y, Onodera Y, Kuroiwa M, Nomimura S, Kubo Y, Nam JM, Kajiwara K, Nada S, Oneyama C, Sabe H, Okada M.
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Journal Title
Oncogenesis
Volume: 5
Issue: 9
Pages: e258-e258
DOI
Related Report
Peer Reviewed / Open Access / Acknowledgement Compliant
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[Journal Article] P53- and mevalonate pathway-driven malignancies require Arf6 for metastasis and drug resistance2016
Author(s)
Hashimoto A, Oikawa T, Hashimoto S, Sugino H, Yoshikawa A, Otsuka Y, Handa H, Onodera Y, Nam JM, Oneyama C, Okada M, Fukuda M, Sabe H
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Journal Title
J Cell Biol
Volume: 213
Pages: 81-95
NAID
Related Report
Peer Reviewed / Acknowledgement Compliant
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[Journal Article] Polarization of M2 macrophages requires Lamtor1 that integrates cytokine and amino-acid signals2016
Author(s)
Kimura T, Nada S, Takegahara N, OkunoT, NojimaS, Kang S, Ito D, Morimoto K, Morimoto K, Hosokawa T, Hayama Y, Mitsui Y, Sakurai N, Sarashina-Kida H, Nishide M, Maeda Y, Takamatsu H, Okuzaki D, Yamada M, Okada M, Kumanogoh A.
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Journal Title
Nat Commun.
Volume: 7
Issue: 1
Pages: 13130-13130
DOI
Related Report
Peer Reviewed / Open Access
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