DJ-1 regulating anticancer resistance through suppressing p53

2015 Fiscal Year Final Research Report

• Project/Area Number: 25830071
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Tumor biology
• Research Institution: Hokkaido University
• Principal Investigator: KATO Izumi 北海道大学, 薬学研究科(研究院), 助教 (40634994)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: DJ-1 / p53 / がん

Outline of Final Research Achievements

The effect of cancer cell death increases depending on the ROS (Reactive Oxygen Species) in pancreatic cancer cells after anti-cancer therapy. DJ-1 binds to p53 and suppresses the transactivation activity of p53 depending on the p53-DNA binding affinity. The survival rate of pancreatic cancer patients who express high level of DJ-1 reduces by half. Therefore, cell death suppression by oxidative stress was predicted to work the malignant alteration of pancreatic cancer. We revealed the interaction between anticancer drug resistance and DJ-1. Furthermore, the relationship between anticancer drug resistance and DJ-1 or p53 was estimated by using the pancreatic cancer cells with different anticancer drug resistance.

Free Research Field

細胞生物学