| Project/Area Number |
15K19332
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Gastroenterology
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| Research Institution | The University of Tokushima |
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Principal Investigator |
KIMURA Tetsuo 徳島大学, 大学院医歯薬学研究部(医学系), 助教 (30564489)
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| Research Collaborator |
TAKEHARA Masanori 徳島大学, 病院, 医員
TAKAYAMA Tetsuji 徳島大学, 大学院医歯薬学研究部, 教授
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 膵癌 / 脂肪細胞 / 腫瘍微小環境 / 細胞間相互作用 |
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| Outline of Final Research Achievements |
Pancreatic cancer cells come into close contact with adipocytes in the retroperitoneal fat tissue at the tumor invasive front. However, the role of these adipocytes in pancreatic cancer progression remains unclear. We show that adipocytes co-cultivated with human pancreatic cancer cells (panc-1) exhibit an altered phenotype in terms of delipidation, decreased adipocyte markers, and increased expression of fibroblast marker (S100A4). Likewise, human pancreatic cancer cells co-cultivated with these morphologically changed adipocytes, termed as cancer associated adipocyte (CAA), exhibited increased invasive capacity and mobility. Microarray analysis of panc-1 cultivated with conditioned media from CAA showed 78.5-fold overexpression of serum amyloid A1 (SAA1). Our data suggest that SAA1 played a key role in the acquired proinvasive effect in tumor cells. These data indicate that crosstalk between tumor cells and adipocytes contribute to the highly malignant potential of pancreatic cancer.
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