2023 Fiscal Year Final Research Report
HOXB9 induces EMT and angiogenic factor for pancreatic cancer
| Project/Area Number |
21K08694
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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 55020:Digestive surgery-related
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| Research Institution | Tokyo Medical University |
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Principal Investigator |
Chiba Naokazu 東京医科大学, 医学部, 准教授 (90348665)
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| Project Period (FY) |
2021-04-01 – 2024-03-31
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| Keywords | HOXB9 / 膵癌 |
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| Outline of Final Research Achievements |
The percentage of viable cells in siHoxB9-transfected cells was lower than in control cells under anticancer drug treatment. Pancreatic cancer stem cell markers were also decreased by siHOXB9-transfected cells. Furthermore, together with the aforementioned results, it was confirmed that the changes in TGFb signature, angiogenic factors, and EMT markers caused by siHOXB9 transfection were all reversed by TGFb recombinant administration.
Comparison of HoxB9 expression and TGFb signature in pancreatic cancer resected specimens showed that most TGFb signatures were positively correlated with HOXB9.
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| Free Research Field |
Surgical Oncology
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| Academic Significance and Societal Importance of the Research Achievements |
今回の研究で明らかにした膵癌細胞におけるメカニズムの鍵となるHOXB9の働きはTGFb経路を介してEMT変化を引き起こすことで、癌の悪性度や治療抵抗性の有無などの質的診断ができる可能性があると考える。今後さらなる詳細なメカニズムが解明され、HOXB9を人為的に制御可能となれば、癌細胞をMesenchymal-Epitherial-Transition（MET）化することによって治療効果を向上させる可能性につながる。今後の研究でこれまでの根治が困難とされてきた癌治療の限界を克服でき、新たな治療法の開発にもつながることが期待される。
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