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

Abstract

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