2018 Fiscal Year Final Research Report
Analysis of plasticity of cancer-initiating cells in malignant tumors
| Project/Area Number |
16K08649
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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 |
Human pathology
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| Research Institution | Chiba University (2018)
Osaka University (2016-2017) |
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Principal Investigator |
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Keywords | 腫瘍幹細胞 / 病理学 / 子宮内膜癌 / アルデヒド脱水素酵素 / 可塑性 |
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| Outline of Final Research Achievements |
RNA-seq analysis was performed on cells in a state in which cancer-initiating cells (CICs) were likely to cause plasticity and in a state in which CICs were not easily induced using endometrioid carcinoma cell lines. Glycoprotein M6B (GPM6B) found in a state in which plasticity was likely to occur was immunohistochemically expressed in agreement with the ALDH-positive area in endometrioid carcinoma cases. When sarcosine, which was produced from glycine by glycine N-methyltransferase, which was expressed in a state that was difficult to induce CICs, was administered to cancer cell lines, the proportion of cells with high ALDH activity was decreased in a concentration-dependent manner. It was suggested that these factors might be involved in the control of CIC plasticity.
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| Free Research Field |
医歯薬学
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| Academic Significance and Societal Importance of the Research Achievements |
腫瘍の中には化学療法や放射線療法に抵抗性で，再発や転移の原因になるとされる「腫瘍幹細胞」と呼ばれる細胞群が存在し，「腫瘍幹細胞」の制御ががん治療の重要な鍵となっている．従来，「腫瘍幹細胞」から「腫瘍幹細胞」と「非腫瘍幹細胞」が生み出され，「非腫瘍幹細胞」から「腫瘍幹細胞」にはならないとされてきたが，「非腫瘍幹細胞」が「腫瘍幹細胞」に転換しうる「可塑性」を有することが報告され，治療を考える上でより複雑な状況になってきている．この可塑性のメカニズムを解明することでがん治療への応用につながる可能性があり，本研究成果は学術的にも社会的にも意義あるものと考える．
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