Molecular mechanism of radio-sensitization by redox modification in cancer cells

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K09991
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Radiation science
• Research Institution: University of Toyama
• Principal Investigator: ZHAO QING-LI 富山大学, 大学院医学薬学研究部(医学), 助教 (90313593)
• Research Collaborator: Li Peng
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: 細胞死 / 放射線 / 温熱

Outline of Final Research Achievements

In this study, the efficacy of some compounds was investigated to modify radiation or hyperthermia induced cell death. Lysolipin I or BU-4664L induced apoptosis in U937 and Molt-4 cells. In addition, Lisolipin I also enhanced radiation-induced apoptosis while, the low concentration BU-4664L have a protecting effect on radiation induced apoptosis. In this study, we determined that Tempo combine treatment with hyperthermia rapidly induced autophagic cell death. Tempo 5 mM -44℃/20 min combination induced apoptosis, while Tempo 5 mM -44℃/60 min combination induced autophagic cell death in HeLa cells. This co-treatment inhibited the processing of heat-activated procaspase-3 into active small subunits, leading to the inhibition of caspase-dependent apoptosis, and results in the induction of autophagic cell death. Furthermore, the gene chip analysis showed the up-regulation of TP53INP1 and cyclin-dependent kinase inhibitor (CDKI) genes in the combination treatment.

Free Research Field

放射線医学