Study of the suppressor protein of cancer cell invasion
| Project/Area Number |
16K07165
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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 |
Tumor therapeutics
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| Research Institution | Kanazawa University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
尾山 武 金沢大学, 医学系, 助教 (00515314)
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2018: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2017: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2016: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 浸潤 / 細胞移動 / 乳癌 / NELL / 接着 / 癌 / 抑制 |
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| Outline of Final Research Achievements |
In this study, we demonstrated the expression and function of Neural EGFL like (NELL), which is a secretory protein in breast tissues. NELL2 was expressed in the myoepithelial cells, and Roundabout Guidance Receptor 3 (ROBO3), which is one of the receptors of NELL2, was expressed in the luminal epithelial cells and breast cancer cells. From the breast ductal structure that composed inside of the luminal epithelial cells and outside of the myoepithelial cells, we suspected the distribution of these cells by ligand (NELL2)-receptor (ROBO3) repulsion. N-terminal thrombospondin-like (TSP) domain contained constructs were bound the surface of breast cancer cell lines. Full-length NELL2 and c-terminal deleted NELL2 construct suppressed the breast cancer cell migration in vitro, however, TSP domain alone was increased migrated cells. It might be suggested that TSP domain of NELL2 related to the binding on the surface of breast cancer cells, but not enough for the cell repulsive signal.
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| Academic Significance and Societal Importance of the Research Achievements |
癌細胞の移動を抑制する因子を明らかにすることは、細胞の生物学的特性を明確にするのみならず、癌の浸潤や転移を阻害する薬剤などの開発につながる可能性がある。また、正常乳管の乳管上皮細胞におけるレセプターと、筋上皮細胞におけるリガンドの発現は、異なる細胞の住み分けや位置づけがレセプター・リガンドの反発作用により誘導されていると推測され、正常乳管の構造形成解明の一助となると考えている。
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Report
(4 results)
Research Products
(4 results)
