論文 - 詳細
| RRC ID | 78747 |
|---|---|
| 著者 | Tomii A, Higa M, Naito K, Kurata K, Kobayashi J, Takei C, Yuasa K, Koto Y, Shimizu H. |
| タイトル | Activation of the TLR4-JNK but not the TLR4-ERK pathway induced by indole-3-acetic acid exerts anti-proliferative effects on Caco-2 cells. |
| ジャーナル | Biosci Biotechnol Biochem |
| Abstract |
We previously found that indole-3-acetic acid (IAA) produced from tryptophan by gut microbiota decreases the expression of tumor necrosis factor α (TNFα), which is implicated in the pathogenesis of colorectal cancer (CRC). The present study aimed to determine IAA involvement in the proliferation of CRC-derived Caco-2 cells. Cell proliferation was suppressed by IAA, whereas IAA-induced aryl hydrocarbon receptor activation had no impact. IAA activated extracellular signal-related (ERK) and c-Jun N-terminal (JNK) kinases, but not p38. Toll-like receptor 4 (TLR4) may be required to activate ERK and JNK, but only the TLR4-JNK pathway might elicit the anti-proliferative effects of IAA. Thus, IAA may be a ligand for TLR4 that contributes to inhibiting CRC cell proliferation by activating TLR4-mediated JNK. Because IAA did not induce cytotoxicity, inhibiting cell cycle progression might affect the anti-proliferative capacity of IAA. Therefore, colonic IAA accumulation might help to prevent CRC development and progression. |
| 巻・号 | 87(8) |
| ページ | 839-849 |
| 公開日 | 2023-7-24 |
| DOI | 10.1093/bbb/zbad055 |
| PII | 7153323 |
| PMID | 37147026 |
| MeSH | Caco-2 Cells Humans JNK Mitogen-Activated Protein Kinases / metabolism MAP Kinase Signaling System* Toll-Like Receptor 4* / metabolism p38 Mitogen-Activated Protein Kinases / metabolism |
| IF | 1.516 |
| オルトメトリクス指標 |
オルトメトリクス指標項目
|
| 最多言及媒体 | X(Twitter) |
| 各媒体での言及数の合計 | 3 |
| 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 | CACO-2(RCB0988) |