| Project/Area Number |
26670141
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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 |
General medical chemistry
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| Research Institution | Kyoto University |
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Principal Investigator |
ENOMOTO Masato 京都大学, 生命科学研究科, 特定助教 (00596174)
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 細胞競合 / 適応度 / JNK / Hippo経路 / がん / JNKシグナル / 細胞適応度 / がん進展 |
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| Outline of Final Research Achievements |
JNK signaling has long been recognized as a dual-functional oncogenic signaling that exerts both anti- and pro-tumor activities. However, the mechanisms by which JNK signaling switches its oncogenic roles in different cellular contexts are poorly understood. In this study, we found that JNK signaling also suppressed cell proliferation of these oncogenic clone. Mechanistically, JNK signaling inhibited the transcriptional coactivator Yorkie(Yki) through Warts(Wts) activation, thereby suppressed tumor growth. Interestingly, in cells with elevated Ras activities, JNK signaling induced F-actin accumulation through Ajuba protein by cooperation of Ras signaling. Changing F-actin dynamics leads to activate Yki through Wts inactivation, thereby induced tumor overgrowth. Our findings reveal that JNK signaling controls tumor progression by switching the Hippo pathway activity.
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