| Project/Area Number |
24591971
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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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| Research Field |
Digestive surgery
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| Research Institution | Suzuka University of Medical Science |
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Principal Investigator |
YONEDA Misao 鈴鹿医療科学大学, 保健衛生学部, 准教授 (60600492)
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| Co-Investigator(Kenkyū-buntansha) |
SHIRAISHI Taizo 三重大学, 大学院医学系研究科, 教授 (30162762)
HIROKAWA Yoshifumi 三重大学, 大学院医学系研究科, 講師 (30322738)
ISHII Kenichiro 三重大学, 大学院医学系研究科, 助教 (90397513)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2012: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 大腸癌 / 化学療法薬耐性獲得 / 腫瘍関連マクロファージ / 癌幹細胞ニッチ / IL1B / ナフトピジル / スフェロイド形成 / IL-1beta / フェニルピペラジン誘導体 / 細胞周期阻害作用 / alpha1アドレナリン受容体 |
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| Outline of Final Research Achievements |
In the tumor microenvironment, tumor-associated macrophages (TAMs) are considered to play a critical role in the regulation of cancer stem/initiating cells. In this study, we hypothesized that TAMs may be involved in the response to chemotherapy. To explore the effective drug for inhibiting induction of TAMs-like differentiation in normal macrophages s by cancer cells, we performed in vitro co-culture experiments. In in vitro co-culture of PMA-THP-1 cells with human colon cancer cell lines, IL1B mRNA was upregulated by co-culturing with HT29 cells. Among 4 phenylpiperazine derivatives, only naftopidil showed anti-proliferative activity on human colon cancer cell lines. Induction of TAMs-like differentiation in PMA-THP-1 cells by co-culturing with HT29 cells was completely cancelled by naftopidil. Our data suggested strongly that naftopidil might be effective in inhibiting induction of TAMs-like differentiation in normal macrophages by colon cancer cells.
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