非瑟酸抑制 Ishikawa 子宫内膜癌细胞增殖并下调 Toll 样受体通路基因的表达。

Fusaric acid inhibits cell proliferation and downregulates expressions of toll-like receptors pathway genes in Ishikawa endometrial cancer cells.

机构信息

Department of Medical Biology, Faculty of Medicine, Ordu University, Ordu, Turkey.

出版信息

Eur Rev Med Pharmacol Sci. 2023 Aug;27(16):7431-7436. doi: 10.26355/eurrev_202308_33394.

DOI:10.26355/eurrev_202308_33394

PMID:37667919

Abstract

OBJECTIVE

Fusaric acid is a derivative of picolinic acid produced by some Fusarium species. In this study, we aimed to determine the mRNA expression and antiproliferative effects of fusaric acid in Ishikawa endometrium cancer cells in signal pathway genes associated with Toll-like receptors (TLRs). The effect of fusaric acid on the viability of Ishikawa cells was evaluated using XTT.

PATIENTS AND METHODS

After total RNA was isolated from control and dose group cells, cDNA synthesis was performed, and mRNA expression changes of genes involved in the Toll-like signaling pathway were evaluated by real-time reverse-transcription polymerase chain reaction (RT-PCR).

RESULTS

The decrease in viability of Ishikawa cells was observed in a time- and dose-dependent manner. The inhibitory concentration (IC50) dose of fusaric acid at the 72nd hour in the Ishikawa cell line was 142.81 µM. When the dose group treated with 125 µM fusaric acid at the 72nd hour was compared with the control group, significantly decreased toll-like receptor 1 (TLR1), TLR2, TLR3, TLR4, TLR5, TLR6, TLR7, TLR8, TLR9, TLR10, and Myeloid differentiation primary response protein 88 (MYD88) gene expressions were observed.

CONCLUSIONS

Fusaric acid inhibits cell proliferation and downregulates Toll-like receptors pathway gene expression in Ishikawa endometrial cancer cells.

摘要

目的

呋咱酸是某些镰刀菌属产生的一种吡啶羧酸衍生物。在这项研究中，我们旨在确定与 Toll 样受体（TLR）相关信号通路基因中呋咱酸在子宫内膜癌细胞系 Ishikawa 中的 mRNA 表达和抗增殖作用。使用 XTT 评估呋咱酸对 Ishikawa 细胞活力的影响。

患者和方法

从对照组和剂量组细胞中分离总 RNA 后，进行 cDNA 合成，并通过实时逆转录聚合酶链反应（RT-PCR）评估 Toll 样信号通路相关基因的 mRNA 表达变化。

结果

Ishikawa 细胞活力呈时间和剂量依赖性下降。在 Ishikawa 细胞系中，72 小时时呋咱酸的抑制浓度（IC50）剂量为 142.81 µM。与对照组相比，在 72 小时时用 125 µM 呋咱酸处理的剂量组，TLR1、TLR2、TLR3、TLR4、TLR5、TLR6、TLR7、TLR8、TLR9、TLR10 和髓样分化初级反应蛋白 88（MYD88）基因表达明显降低。