| Budget Amount *help |
¥14,820,000 (Direct Cost: ¥11,400,000、Indirect Cost: ¥3,420,000)
Fiscal Year 2012: ¥3,250,000 (Direct Cost: ¥2,500,000、Indirect Cost: ¥750,000)
Fiscal Year 2011: ¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2010: ¥7,410,000 (Direct Cost: ¥5,700,000、Indirect Cost: ¥1,710,000)
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| Research Abstract |
Increasing evidence suggests that tumor-initiating cells (TIC) contribute to the development of prostate cancer. We identify syndecan-1 as a key molecule for maintaining the stability of prostate cancer TIC. Holoclones harboring biological properties of stemness overexpressed syndecan-1, but showed reduced expression of NADPH oxidase and synthesis of hydrogen peroxide and oxygen radicals. In the transgenic adenocarcinoma of the mouse prostate (TRAMP) model of prostate cancer, early intervention with a syndecan-1 inhibitor (OGT2115) or syndecan-1 RNAi reduced the cancer incidence and the number of c-kit+/CD44+ cells. Syndecan-1 immunopositivity in prostate cancer cells was significantly associated with biochemical recurrence after radical prostatectomy. Taken together, syndecan-1 contributes to prostatic carcinogenesis by maintaining TIC, and might be a novel target molecule for effective cancer therapy.
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