Functional analyses of Crumbs3 as the moleculer switch of cell-matrix adhesion in colon cancer progression
Project/Area Number |
17K08737
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Human pathology
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Research Institution | Niigata University |
Principal Investigator |
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Co-Investigator(Kenkyū-buntansha) |
近藤 英作 新潟大学, 医歯学系, 教授 (30252951)
|
Project Period (FY) |
2017-04-01 – 2020-03-31
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Project Status |
Completed (Fiscal Year 2019)
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Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2019: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2018: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2017: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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Keywords | 細胞極性 / 浸潤転移 / FGFR / 大腸癌 / metastasis / polarity / Crumbs3 / 腫瘍 / 浸潤 / 転移 / 細胞・組織 / 病理学 / 遺伝子 / 癌 |
Outline of Final Research Achievements |
Transmembrane protein Crumbs3 is expressed in the epithelial tissues. Previous reports indicated that Crumbs3 is not only functions as an essential regulator for normal epithelial development but also a tumor suppressor in model organisms. In this study, the details of the expression and function of Crumbs3 in human malignant tumors were analyzed, and we found Crumbs3 is strongly expressed in the adenocarcinomas. Furthermore, we demonstrated that Crumbs3, which is formerly described as a tumor suppressor, promotes metastasis in colon adenocarcinoma cells.
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Academic Significance and Societal Importance of the Research Achievements |
本邦における国民の死因第一位は「悪性腫瘍」であり、悪性腫瘍の転移は患者の予後を左右する最も大きな要因の一つである。浸潤転移の激しい難治がん、進行がんに対しては未だ有効な手立てが無く、がんの性状解析に基づく新たな治療戦略の提案が求められている。本研究ではこれまでがん抑制因子と考えられてきたCrumbs3というタンパク質に着目し、ヒトの大腸癌サンプルを用いた解析を行った。その結果、Crumbs3が大腸癌の転移を促進すること、および、その制御メカニズムの一端が明らかとなった。今後、Crumbs3とその関連分子を標的とすることで、新たな転移の診断・治療法の開発につながる可能性がある。
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Report
(4 results)
Research Products
(11 results)