| Project/Area Number |
15H04943
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Respiratory surgery
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| Research Institution | Osaka University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
南 正人 大阪大学, 医学部附属病院, 准教授 (10240847)
川村 知裕 大阪大学, 医学系研究科, 助教 (30528675)
奥村 明之進 大阪大学, 医学系研究科, 教授 (40252647)
舟木 壮一郎 大阪大学, 医学系研究科, 講師 (50464251)
井上 匡美 京都府立医科大学, 医学(系)研究科(研究院), 教授 (10379232)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥16,770,000 (Direct Cost: ¥12,900,000、Indirect Cost: ¥3,870,000)
Fiscal Year 2017: ¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
Fiscal Year 2016: ¥6,110,000 (Direct Cost: ¥4,700,000、Indirect Cost: ¥1,410,000)
Fiscal Year 2015: ¥7,280,000 (Direct Cost: ¥5,600,000、Indirect Cost: ¥1,680,000)
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| Keywords | 肺癌 / 癌周囲微小環境 / 上皮間葉移行 / 癌幹細胞 / 癌関連線維芽細胞 / 抗線維化剤 / IL-6 / TGF-β / 癌幹細胞様形質 / 肺癌治療 / 薬剤耐性 |
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| Outline of Final Research Achievements |
The tumor microenvironment is composed of different types of stromal cells that represent a key component of tumor progression. We have reported that TGF-β signaling mediates epithelial mesenchymal transition (EMT) in non-small-cell lung cancer (NSCLC) cells. In order to identify new targets for prevention of metastasis, it is important to understand the molecular mechanisms that drive EMT. Interaction between cancer-associated fibroblasts (CAFs) and tumor cells have shown increased tumor cell survival via several pathways including EMT. We showed that IL-6 from CAFs enhanced TGF-β induced EMT in NSCLC cells. Furthermore, an anti-fibrotic agent significantly inhibited production of IL-6 or TGF-β1 of CAFs, resulting in inhibition of the EMT change in NSCLC cells. In in vivo examination, the anti-fibrotic agent also suppressed the tumor progression. Targeting CAFs as a therapeutic strategy against cancer is an intriguing concept that would benefit from further study.
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