| Project/Area Number |
22240090
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| Research Category |
Grant-in-Aid for Scientific Research (A)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Tumor diagnosis
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| Research Institution | Tokyo Medical and Dental University |
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Principal Investigator |
INAZAWA Johji 東京医科歯科大学, 難治疾患研究所, 教授 (30193551)
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| Co-Investigator(Kenkyū-buntansha) |
KOZAKI Kenichi 東京医科歯科大学, 難治疾患研究所, 准教授 (50270715)
INOUE Jun 東京医科歯科大学, 難治疾患研究所, 助教 (50568326)
井本 逸勢 徳島大学, 大学院・ヘルスバイオサイエンス研究部, 教授 (30258610)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥50,180,000 (Direct Cost: ¥38,600,000、Indirect Cost: ¥11,580,000)
Fiscal Year 2012: ¥13,130,000 (Direct Cost: ¥10,100,000、Indirect Cost: ¥3,030,000)
Fiscal Year 2011: ¥15,990,000 (Direct Cost: ¥12,300,000、Indirect Cost: ¥3,690,000)
Fiscal Year 2010: ¥21,060,000 (Direct Cost: ¥16,200,000、Indirect Cost: ¥4,860,000)
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| Keywords | 難治がん / 癌遺伝子 / 癌抑制遺伝子 / ゲノム / エピゲノム / マイクロRNA / DNAメチル化 / 分子標的薬 |
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| Research Abstract |
In order to develop useful diagnostic tools for personalized cancer medicine, we performed genetic and epigenomic analyses in cancer, and identified novel cancer-related genes. By using methylation-based screening of tumor suppressor (TS) -miRNAs in oral squamous cell carcinoma (OSCC), we identified miR-596 and it target gene, LGALS3BP. Epithelial-mesenchymal transition (EMT) is relevant to the mechanism of invasion and metastasis in cancer. From a comprehensive gene expression analysis using colorectal cancer (CRC) cell lines, and following the ontology (GO) analysis, SIX1 was identified as an EMT-related gene in CRC. Furthermore, through DNA methylation and gene expression analyses of components in the Wnt signaling pathway, we identified WNT7A and WNT10A as genes silenced by mesenchymal-specific DNA hypermethylation in oral OSCC. In autophagy LC3 has a physiologically important role. Among LC3 family genes, we identified two transcriptional variants of LC3A, LC3Av1 and LC3Av2. Interestingly, we found that LC3Av1 functions in autophagy and indicated that LC3Av1 may be crucial in various types of cancer.
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