2015 Fiscal Year Final Research Report
Functional analysis of autophagy in PTEN/Atg7 double knockout mouse prostate cancer
Project/Area Number |
26670707
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Research Category |
Grant-in-Aid for Challenging Exploratory Research
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Allocation Type | Multi-year Fund |
Research Field |
Urology
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Research Institution | Kinki University |
Principal Investigator |
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Project Period (FY) |
2014-04-01 – 2016-03-31
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Keywords | オートファジー / 前立腺癌 / マウスモデル / ノックアウトマウス / PTEN / Cre-LoxPシステム / 去勢抵抗性がん / Atg7 |
Outline of Final Research Achievements |
We had previously developed a conditional knockout mouse model in which homozygous deletion of PTEN lead to the stage-specific development of invasive adenocarcinoma. To determine the effect of defective autophagy on prostate cancer progression, we generated prostate-specific conditional double knockout mice harboring both inactivated PTEN and ATG7, a key regulator for the formation of autophagosomes. We show that inhibition of autophagy by the conditional inactivation of ATG7, a gene essential for autophagosome formation, does not contribute to tumor initiation. We also show that simultaneous inactivation of ATG7 significantly suppresses PTEN-deficient prostate cancer progression and improves survival.
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Free Research Field |
泌尿器腫瘍学
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