| Project/Area Number |
25893093
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Obstetrics and gynecology
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| Research Institution | Nagoya University |
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Principal Investigator |
SEKIYA RYUICHIRO 名古屋大学, 医学(系)研究科(研究院), 特任助教 (40712352)
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| Project Period (FY) |
2013-08-30 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | PLAGL2 / 卵巣癌 / RhoA / Rac1 / 転移 / Rho / Rac / 上皮間葉転換 / 腹膜播種 |
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| Outline of Final Research Achievements |
Pleomorphic adenoma gene like-2 (PLAGL2), a member of the PLAG gene family, is a C2H2 zinc finger transcriptional factor that is involved in cellular transformation and apoptosis. We found that PLAGL2 depletion induced organization of stress fibers. In addition, formation of focal adhesions was promoted by PLAGL2 knockdown. Rac1 was inactivated in the absence of PLAGL2, whereas activity of RhoA was increased. Conversely, exogenous expression of PLAGL2 induced disruption of stress fiber formation and production of lamellipodia. Consistently, RhoA was suppressed and Rac1 was activated by PLAGL2 overexpression. PLAGL2 expression induced lamellipodia formation and disruption of stress fiber formation. Finally, we show that chimerin1(CHN1) expression is essential for Rac1 inactivation in PLAGL2-depleted cells.
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