2022 Fiscal Year Final Research Report
Elucidation of mechanotransduction mechanisms in oral squamous cell carcinoma cells with high CD44 expression
| Project/Area Number |
20K10138
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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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| Review Section |
Basic Section 57060:Surgical dentistry-related
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| Research Institution | Hiroshima University |
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Principal Investigator |
Shigeishi Hideo 広島大学, 医系科学研究科(歯), 講師 (90397943)
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| Co-Investigator(Kenkyū-buntansha) |
小野 重弘 広島大学, 医系科学研究科(歯), 助教 (70379882)
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| Project Period (FY) |
2020-04-01 – 2023-03-31
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| Keywords | 癌幹細胞 / CD44 / アポトーシス抵抗性 / メカニカルストレス |
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| Outline of Final Research Achievements |
Cofilin-1, an intracellular actin-modulating protein, was involved in the invasive capacity of CD44high OSCC cells. TGF-β1 induced amoeboid-to-mesenchymal transition by Cofilin-1 phosphorylation and downregulation of miR-422a via ERK activation. Our findings suggest that miR-422a and Cofilin-1 play major roles in the maintenance of amoeboid-like CD44high cells. Furthermore, miR-224-5p plays a vital role in the resistance to docetaxel-induced apoptosis by attenuating PANX1-induced ATP discharge.
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| Free Research Field |
外科系歯科学
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| Academic Significance and Societal Importance of the Research Achievements |
amoeboid-like CD44高発現口腔扁平上皮癌細胞は、高い浸潤能を持つことから、腫瘍の再発や転移に関与している可能性が示唆された。さらに、amoeboid-like CD44高発現口腔扁平上皮癌細胞は、口腔扁平上皮癌における抗がん剤抵抗性に関与していると予測されるため、amoeboid-like CD44高発現口腔扁平上皮癌細胞におけるアポトーシス回避機構を解明することが重要であると考えられた。
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