| Budget Amount *help |
¥11,310,000 (Direct Cost: ¥8,700,000、Indirect Cost: ¥2,610,000)
Fiscal Year 2009: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
Fiscal Year 2008: ¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2007: ¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
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| Research Abstract |
Strategy for targeted cancer therapies are based on analysis of signal mechanism involved in cell growth and cell death. In malignant glioma cells, conventional chemotherapeutic agents not only induce apoptosis in cancer cells, but other types of cell death referred to as programmed cell death type II which morphologically features and characterized by autophagic vesicles in the cytoplasm without chromatin condensation. In cancer research, autophagy has been considered to be a novel concept and here, we analyzed that autophagy in cell death is regulated by molecular machinery. Our analyses using malignant glioma cells have showed that BNIP3 were up-regulated in autophagic cell death after cytopathic anticancer treatments with up-regulation of its binding partners Bcl-2. Intersetingly, inhibition of Bc-2 enhanced cytotoxic effect of anticancer treatments. These results indicate that association of BNIP3 and Bcl-2 regulates defensive or destructive autophagy and modulation of molecular machinery of autophagy is expected to enhance the cytotoxicity of anticancer treatments for malignant gliomas.
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