| Project/Area Number |
22791507
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Urology
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| Research Institution | Chiba Cancer Center (Research Institute) |
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Principal Investigator |
TATSUMI Yasutoshi 千葉県がんセンター(研究所), 研究所 がんゲノム研究室, 研究員 (00450578)
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| Project Period (FY) |
2010-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2013: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2012: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2011: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2010: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
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| Keywords | 前立腺がん / BMCC1蛋白質 / アポトーシス促進因子 / siRNA / ノンコーディングRNA / 前立腺癌 / BMCC1タンパク質 |
|---|
| Research Abstract |
The Long non-coding RNA, DD3, gene was mapped at the intron 6 within BMCC1 gene in an opposite way. In prostate cancer cell lines, there occurred inverse regulation in BMCC1 and DD3 expression. These suggested that DD3 targets BMCC1 for its expression to be decreased in prostate cancer cells. In contrast to higher expression of DD3 in prostate cancer tissues, lower expression of BMCC1 in primary prostate cancers in compared with corresponding normal tissues were detected by immunohistochemistry using anti-BMCC1 antibody. In addition, we found that BMCC1 is a key facilitator of mitochondrial apoptosis and DNA damage-induced drug sensitivity through AKT attenuation and associates with Bcl-2. Because DD3 knockdown facilitated the reduction of cell viability and promotion of Cisplatin sensitivity through pro-apoptotic BMCC1 accumulation, we proposed that combination therapy with DD3 siRNA and Cisplatin would be of potential value for treating DD3 positive aggressive prostate cancer.
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