Molecular basis of non-genetic tumor progression through cell-cell communication
| Project/Area Number |
23650596
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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 |
Tumor biology
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| Research Institution | Kobe University |
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Principal Investigator |
IGAKI Tatsushi 神戸大学, 大学院・医学研究科, 客員教授 (00467648)
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2011: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 癌 / シグナル伝達 / 細胞間相互作用 / 細胞・組織 / がん / Ras / ミトコンドリア / 遺伝学 / ショウジョウバエ |
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| Research Abstract |
Mitochondrial respiratory function is frequently impaired in human cancers. However, the mechanisms by which mitochondrial dysfunction contributes to tumor progression remain elusive. We found in Drosophila imaginal epithelium that defects in mitochondrial function potently induce tumor progression of surrounding tissue in conjunction with oncogenic Ras. Ras activation and mitochondrial dysfunction cooperatively stimulate production of reactive oxygen species (ROS), which causes activation of JNK signaling. JNK cooperates with oncogenic Ras to inactivate the Hippo pathway, leading to upregulation of its targets Unpaired (Upd, an IL-6 homolog) and Wingless (Wg, a Wnt homolog). Mitochondrial dysfunction in Ras-activated cells further cooperates with Ras signaling in neighboring cells with normal mitochondrial function, causing benign tumors to exhibit metastatic behavior.
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Report
(3 results)
Research Products
(89 results)
