| Budget Amount *help |
¥328,800,000 (Direct Cost: ¥328,800,000)
Fiscal Year 2009: ¥66,100,000 (Direct Cost: ¥66,100,000)
Fiscal Year 2008: ¥66,100,000 (Direct Cost: ¥66,100,000)
Fiscal Year 2007: ¥66,300,000 (Direct Cost: ¥66,300,000)
Fiscal Year 2006: ¥66,300,000 (Direct Cost: ¥66,300,000)
Fiscal Year 2005: ¥64,000,000 (Direct Cost: ¥64,000,000)
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| Research Abstract |
A series of experiments focusing on the aPKC-PAR complex revealed (1) the new role of PAR1 on the recruitment and organization of extracellular laminin through utrophin/dystroglucan complex. We have also identified ASPP2, known as a mediator of apoptic function of p53, as a partner of the aPKC-PAR complex. (2) In mammary epithelial stem/progenitor cells the aPKC-ErbB2 pathway negatively regulates proliferation. (3) Relationships between aPKC overexpression and the recurrence of prostate cancer, metastasis of stomach cancer, and grade of mammary cancer. Intensive studies on prostate cancer cells revealed the aPKC-IL6 axis. These results reinforce the importance of the understanding of cell polarity for the understanding of cancer cells.
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