| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2012: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2011: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
|
|---|
| Research Abstract |
Autophagy is a celluar response to adverse environment and stress. Recent evidence suggests that tumor cells induce autophagy during treatment of anticancer drugs. However, the effect of these events on cancer is not known. The aime was to evaluate the effect of p53 status and autophagy activity on the chemosensitivity of colorectal cancer.
1.Autophagy was induced in response to DNA damage in p53 wild-type and p53 knockdown(p53-KD) colorectal cancer cells. The accumulation of LC-II was more intense in p53-KD cell than that in p53-cont cell. Furtheremore, we confirmed that apoptosis was induced in response to DNA damage in p53-cont and p53-KD cells after treating with siATG5. Apoptosis in p53-KD cell was less than that in p53-cont cell.
2.Immunohistochemical staining of resected liver tumor revealed that hte expression of some autophagic related protein(Protein A) was markedly decreased. Patients in high Protein A expression group was associated with lymphphatic invation.
|
