Identification of hypermethylated genes associated with increased cell proliferation of prostate cancer using DNA demethyation techniques
| Project/Area Number |
15K08392
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Experimental pathology
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| Research Institution | Tohoku University |
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Principal Investigator |
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 前立腺癌 / DNAメチル化 / DNA脱メチル化 / PYCARD / 癌 / ゲノム / 遺伝子 / 発現制御 / アポトーシス / 細胞増殖 / 脱メチル化 / 転写活性化 |
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| Outline of Final Research Achievements |
DNA methylation is associated with the inappropriate transcriptional silencing of cancer-related genes and affects the hallmarks of cancer such as sustaining proliferative signaling, resisting cell death, and activating invasion and metastasis. We found that genome-wide reactivation of hypermethylated genes suppressed growth of prostate cancer cell line LNCaP and induced apoptosis. We searched for apoptosis-inducing genes whose promoters were hypermethylated in prostate cancers. As a result, we found that the promoter region of PYCARD, one of apoptosis-inducing factor, were highly methylated in a cancer-specific manner (46/51: 90%). In addition, PYCARD expression induced apoptosis in LNCaP cells. These results suggest that aberrant promoter hypermethylation of PYCARD plays an important role in prostatic tumorigenesis.
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Report
(4 results)
Research Products
(11 results)
