A study for molecular mechanism of the Cdk-Pin1 axis in cancer stem cell

2014 Fiscal Year Final Research Report

• Project/Area Number: 25830087
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Tumor biology
• Research Institution: Yokohama City University
• Principal Investigator: NISHI Mayuko 横浜市立大学, 医学(系)研究科(研究院), 特任助教 (90635343)
• Project Period (FY): 2013-04-01 – 2015-03-31
• Keywords: 癌幹細胞 / リン酸化 / 癌抑制遺伝子 / 細胞老化

Outline of Final Research Achievements

We recently established an induced cancer stem cell (CSC)-like model. We utilized the cell model for drug screening to inhibit the Cdk-Pin1 axis in CSCs. Withaferin A (WA) was identified as a compound inhibiting Cdk activity by inducing p21. WA inhibited not only the stemness and self-renewal properties of CSCs but also their ability of migration and invasion. WA decreased both the tumor initiation and the tumor-forming ability of CSCs in an immunosuppressed mouse model. We further attempted to identify functional Cdk substarates by a protomic approach using Pin1 as a molecular probe. We indentified several target proteins for further analysis.

Free Research Field

分子腫瘍学