| Project/Area Number |
14370677
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Surgical dentistry
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| Research Institution | KYUSHU UNIVERSITY |
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Principal Investigator |
MORIFUJI Masayo (2004) Kyushu University, University Hospital, Research Associate, 病院, 助手 (90271113)
大石 正道 (2002-2003) 九州大学, 歯学研究院, 教授 (70037505)
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| Co-Investigator(Kenkyū-buntansha) |
NAKABEPPU Yusaku Kyushu University, Medical Institute, Professor, 生体防御医学研究所, 教授 (30180350)
森藤 政代 九州大学, 大学病院, 助手 (90271113)
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| Project Period (FY) |
2002 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥13,900,000 (Direct Cost: ¥13,900,000)
Fiscal Year 2004: ¥2,800,000 (Direct Cost: ¥2,800,000)
Fiscal Year 2003: ¥3,700,000 (Direct Cost: ¥3,700,000)
Fiscal Year 2002: ¥7,400,000 (Direct Cost: ¥7,400,000)
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| Keywords | tumor markers / proteomic analysis / invasion・metastsis / oral cancer / orthotopic implantation / 質量分析法 |
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| Research Abstract |
In order to detect tumor markers we investigated the sputum and serum of patients. We could not determine the quantity of their proteins. So we needed to think how to detect tumor markers in sputum and serum. We concluded that the method by RT-PCR was suitable for sputum, while for serum that by western blotting was. As we can see primary tumor in case of oral cancer, it is significant to detect metastasis or tumors cells obtained the abilities of invasion and metastasis. Tumor tissue was heterogeneous, so we investigated cancer cell lines in order to gain the molecules related to metastasis. By using iTRAQ method, we did proteomic analysis in tongue cancer cell lines that were differences in invasive and metastatic abilities in orthotopic implantation. We identified 163 kinds of by analyzing amino acid. Using oligonucleotide microarray representing 54525 genes, 186 kinds of known genes and 137 kinds of unknown genes were up-regulation, while 147 kinds of known genes and 241 kinds of unknown genes were down-regulation. We show endostatin inhibited lymph node metastasis by the down-regulation of VEGF-C and VEGF-D expression in tumor cells. In addition we established the animal model of heterogeneous tumor and examined heterogeneous cancer development. We found that human Mut T homolog protein 1 (hMTH1) might be related to the growth of metastatic cells. These may be special molecules in metastatic cells. Now we select molecules related to metastasis. This analysis system may give important information to tumor markers and new therapy.
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