2015 Fiscal Year Final Research Report
Roles of ESCRT in Oncogenesis
Project/Area Number |
24300326
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Research Category |
Grant-in-Aid for Scientific Research (B)
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Allocation Type | Partial Multi-year Fund |
Section | 一般 |
Research Field |
Carcinogenesis
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Research Institution | Miyagi Prefectural Hospital Organization Miyagi Cancer Center |
Principal Investigator |
TANAKA NOBUYUKI 地方独立行政法人宮城県立病院機構宮城県立がんセンター(研究所), がん先進治療開発研究部, 部長 (60280872)
|
Co-Investigator(Kenkyū-buntansha) |
OGAMA Naoko 地方独立法人宮城県立病院機構宮城県立がんセンター(研究所), がん先進治療開発研究部, 主任研究員 (30390892)
TAMAI Keiichi 地方独立法人宮城県立病院機構宮城県立がんセンター(研究所), がん幹細胞研究部, 上席主任研究員 (40509262)
Yamaguchi Kazunori 地方独立法人宮城県立病院機構宮城県立がんセンター(研究所), 発がん研究部, 上席主任研究員 (80373215)
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Project Period (FY) |
2012-04-01 – 2016-03-31
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Keywords | ESCRT / 増殖因子受容体 |
Outline of Final Research Achievements |
Vesicular transport is tightly related with oncogenesis, malignant transformation and cell death. In the present study, we analyzed roles of ESCRT in vitro and in vivo. First, we found that ESRT-0 and ESCRT-I both regulate EGFR degradation. Second, AMSH-LP, a deubuiqutination enzyme associated with ESCRT-0 and ESCRT-III, may be involved in oncogenesis, and AMSH-LP knockout mice manifested shorter life span. Third, ESCRT-0 defect did not induce tumor formation, but cells defective for ESCRT-0 showed enhanced necroptosis and apoptosis, partly through the enhanced ER stress. Together, this study showed a pertinent role of ESCRT in cellular growth and death.
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Free Research Field |
腫瘍学
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