| 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
|
| リソース情報 |
| ヒト・動物細胞 |
CACO-2(RCB0988) |
