論文 - 詳細
| RRC ID | 44710 |
|---|---|
| 著者 | Kono Y, Kawakami S, Higuchi Y, Yamashita F, Hashida M. |
| タイトル | In vitro evaluation of inhibitory effect of nuclear factor-kappaB activity by small interfering RNA on pro-tumor characteristics of M2-like macrophages. |
| ジャーナル | Biol Pharm Bull |
| Abstract |
Tumor-associated macrophages (TAMs) have an alternatively activated macrophage phenotype (M2) and promote cancer cell proliferation, angiogenesis and metastasis. Nuclear factor-kappaB (NF-κB) is one of the master regulators of macrophage polarization. Here, we investigated the effect of inhibition of NF-κB activity by small interfering RNA (siRNA) on the pro-tumor response of macrophages located in the tumor microenvironment in vitro. We used mouse peritoneal macrophages cultured in conditioned medium from colon-26 cancer cells as an in vitro TAM model (M2-like macrophages). Transfection of NF-κB (p50) siRNA into M2-like macrophages resulted in a significant decrease in the secretion of interleukin (IL)-10 (a T helper 2 (Th2) cytokine) and a significant increase of T helper 1 (Th1) cytokine production (IL-12, tumor necrosis factor-α, and IL-6). Furthermore, vascular endothelial growth factor production and matrix metalloproteinase-9 mRNA expression in M2-like macrophages were suppressed by inhibition of NF-κB expression with NF-κB (p50) siRNA. In addition, there was a reduction of arginase mRNA expression and increase in nitric oxide production. The cytokine secretion profiles of macrophages cultured in conditioned medium from either B16BL6 or PAN-02 cancer cells were also converted from M2 to classically activated (M1) macrophages by transfection of NF-κB (p50) siRNA. These results suggest that inhibition of NF-κB activity in M2-like macrophages alters their phenotype toward M1. |
| 巻・号 | 37(1) |
| ページ | 137-44 |
| 公開日 | 2014-1-1 |
| DOI | 10.1248/bpb.b13-00659 |
| PII | DN/JST.JSTAGE/bpb/b13-00659 |
| PMID | 24141263 |
| MeSH | Animals Arginase / genetics Arginase / metabolism Cell Line, Tumor Colonic Neoplasms / genetics Colonic Neoplasms / metabolism* Cytokines / metabolism* Interleukins / metabolism Lipopolysaccharides Macrophage Activation Macrophages / metabolism* Macrophages, Peritoneal / metabolism* Matrix Metalloproteinase 9 / metabolism Mice NF-kappa B / antagonists & inhibitors* Neovascularization, Pathologic* Nitric Oxide / metabolism Phenotype RNA, Messenger / metabolism RNA, Small Interfering / metabolism* Signal Transduction Th1 Cells / metabolism Transfection Tumor Necrosis Factor-alpha / metabolism Vascular Endothelial Growth Factor A / metabolism |
| IF | 1.863 |
| 引用数 | 22 |
| WOS 分野 | PHARMACOLOGY & PHARMACY |
| オルトメトリクス指標 |
オルトメトリクス指標項目
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| 最多言及媒体 | X(Twitter) |
| 各媒体での言及数の合計 | 1 |
| 過去6か月間でのオルトメトリクス指標の変動値 | 0.0 |
| リソース情報 | |
| ヒト・動物細胞 | Colon-26(RCB2657) B16/BL6(RCB2638) |