2021 Fiscal Year Final Research Report
Regulation of pancreatic cancer progression by targeting Hic-5, a TGF-beta-inducible adaptor expressed in cancer-stroma.
| Project/Area Number |
19K08404
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Multi-year Fund |
|---|
| Section | 一般 |
|---|
| Review Section |
Basic Section 53010:Gastroenterology-related
|
|---|
| Research Institution | Showa University |
|---|
Principal Investigator |
|
|---|
| Project Period (FY) |
2019-04-01 – 2022-03-31
|
| Keywords | 膵がん / 膵線維化 / がん微小環境 |
|---|
| Outline of Final Research Achievements |
Alteration in the density of extracellular matrix (ECM) occurs in the tumor stroma. We have previously demonstrated that Hydrogen peroxide-inducible clone-5 (Hic-5) was strongly induced in CAFs found in human colorectal cancer and responsible for generating a tumor-promoting stroma. In this study, we focused on pancreatic cancer which is characterized by a dense stromal response, and investigated the contribution of Hic-5 to pancreatic cancer development through regulation of cancer stromal phenotype using a mouse model of pancreatic cancer. Furthermore, we clarified the involvement of Hic-5 in pancreatic fibrosis, which is considered to be one of the causes of pancreatic cancer resistance to treatment.
|
| Free Research Field |
病態医化学
|
| Academic Significance and Societal Importance of the Research Achievements |
膵線維化は難治癌である膵がんの治療抵抗性の一因と考えられており、本研究により膵線維化制御メカニズムの一因が明らかにされた。がん組織中の線維化を標的とした新たな膵がんの治療戦略開発につながるデータである。
|
