2011 Fiscal Year Final Research Report
ILK-GSK3βpathway as a therapeutic target for high risk bladder cancer.
| Project/Area Number |
22890096
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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 |
Urology
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| Research Institution | Kyoto University |
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Principal Investigator |
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| Project Period (FY) |
2010 – 2011
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| Keywords | 転移・浸潤 / インテグリン / 膀胱癌 |
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| Research Abstract |
The aim of the present study was to elucidate the role of Integrin-linked kinase(ILK) in bladder cancer progression, and to explore the possibility of ILK as a therapeutic target for invasive bladder cancer. ILK was up-regulated with tumor progression in chemically induced mouse BBN bladder cancer model, and also in invasive bladder cancer cell lines. ILK increased migration and invasion of bladder cancer cells in vitro, which was associated with down-regulation of E-Cadherin via GSK3β-Zeb1 pathway or up-regulation of MMP9. ILK was up-regulated in invasive bladder cancers in clinical specimen. These data indicate that ILK is associated with bladder cancer progression by inducing epithelial-mesenchymal transition, and that ILK can be a novel therapeutic target in invasive bladder cancer treatment.
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