2013 Fiscal Year Final Research Report
Inhibition of direct metastasis by artificial stabilization of cell-cell adhesion
Project/Area Number |
24700962
|
Research Category |
Grant-in-Aid for Young Scientists (B)
|
Allocation Type | Multi-year Fund |
Research Field |
Tumor biology
|
Research Institution | Akita University |
Principal Investigator |
KURIYAMA Sei 秋田大学, 医学(系)研究科(研究院), 准教授 (30398226)
|
Project Period (FY) |
2012-04-01 – 2014-03-31
|
Keywords | 細胞接着 / 転写制御 / 転移・浸潤 |
Research Abstract |
In cancer, Epithelial-To-Mesenchymal Transition (EMT) is a critical process of metastasis. Mesenchymal cancer cell often expresses cell adhesion molecule, N-cadherin. So far the amounts of N-caherin can't be translated into the increase of malignancy because the malignancy depends on what form of N-cadherin expresses and how it works. In this study, we revealed novel N-cadherin modifiers, Lipoma preferred Partner (LPP), Ets-variant 5, and Metalloproteinase 15, which modify the stabilities of N-cadherin in cancer. We found that loss of LPP in EMT undergone cancer cells further increase the distant metastasis. Therefore, our findings suggest that LPP is one of potential candidate of distant metastasis biomarker, which provide us a better prognosis of N-cadherin positive cancer.
|