2019 Fiscal Year Final Research Report
Analysis of cancer cell malignancy induced by vascular niche signals
| Project/Area Number |
16H02470
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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 biology
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| Research Institution | Osaka University |
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Principal Investigator |
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| Project Period (FY) |
2016-04-01 – 2020-03-31
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| Keywords | 血管新生 / 血管内皮細胞 / ニッチ / がん |
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| Outline of Final Research Achievements |
Based on our previous resources, we analyzed the mechanism of cancer cell metastasis focusing on galectin-3. We found that suppression of galactin-3 induces integrins on cancer cells and promotes cell aggregation with platelets, resulting in enhancement of cancer cell metastasis. In terms of Tie1 tyrosine kinase receptor expressed on endothelial cells in which physiological ligands have not been identified, we found that soluble extra-cellular domain Tie1 receptor which is generated on the onset of angiogenesis, associates with maturation of tumor vasculature. Moreover, by establishing the new co-culture system using cancer cells and endothelial cells, we isolated a novel molecule that can inhibits epithelial to mesenchymal transition.
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| Free Research Field |
腫瘍血管生物学
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| Academic Significance and Societal Importance of the Research Achievements |
正常組織の幹細胞の維持が血管との相互作用により成立している事実と、がん組織のがん幹細胞と血管との関連が明らかにされてきたことから、さらにこの相互作用についての検討を正常組織における組織形成と対比させて考察することにより、がんの悪性化、幹細胞性維持機構が解明できると考え、がん組織のがん細胞と血管形成との相互作用について解析を行い、がんの悪性の進展についての多くの知見が得られてきた。これらの成果に立脚してさらに検討を重ね、新たながん治療薬の開発に貢献できると考えられる。
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