| Budget Amount *help |
¥25,090,000 (Direct Cost: ¥19,300,000、Indirect Cost: ¥5,790,000)
Fiscal Year 2018: ¥8,450,000 (Direct Cost: ¥6,500,000、Indirect Cost: ¥1,950,000)
Fiscal Year 2017: ¥8,450,000 (Direct Cost: ¥6,500,000、Indirect Cost: ¥1,950,000)
Fiscal Year 2016: ¥8,190,000 (Direct Cost: ¥6,300,000、Indirect Cost: ¥1,890,000)
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| Outline of Final Research Achievements |
Although it has been recently shown that distinct oncogenic cell clones heterogeneously exist in cancer tissues, it is still poorly understood how tumor-microenvironment causes cancer progression. To elucidate the underlying mechanism, I recapitulated tumor heterogeneity in Drosophila epithelium and genetically analyzed cell-cell interaction of distinct oncogenic cell populations in vivo. In this research, I found that dying Src-activating cells transform surrounding Ras-activating cells to malignant tumors via cell-cell interaction. Furthermore, I also found that malignant Ras-activating cell clones provide metastatic behaviors to surviving Src-activating cells, thereby two oncogenic cell populations mutually invade the adjacent tissues. These findings suggest that two distinct oncogenic cells mutually develop into malignant tumors via cellular cooperation triggered by dying oncogenic cells.
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