| Budget Amount *help |
¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2013: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
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| Outline of Final Research Achievements |
Cancer cachexia is a highly complex metabolic disorder. Patients exhibit a significant loss of skeletal muscle mass. Recent studies propose the contribution of autophagy-lysosome system to this process. However, its underling mechanisms are still largely unknown. We established an experimental system using human-to-mouse xenotransplantation models of human colorectal cancer to investigate muscle wasting in cahexia. The successfully grew in NOG mice were fixed for immunofluorescence microscopy. An autophagosome marker LC3 was detected as several fine dots in the muscle fibers in control muscle. In tumor-bearing mice, the LC3-dots were significantly increased and often observed as ring or cup-shaped structures, indicating typical autophagosomes. When double-stained with LC3 and p62, p62-dots were largely colocalized with LC3-dots. This study supports the idea that autophagy plays important roles in the muscles wasting in cancer cachexa, and suggests that p62 might mediate this process.
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