Title : Reversal effect of artemisinin on concurrent chemo-radiotherapy via FoxQ1 and the Wnt/?-catenin signaling pathway
Abstract:
This study aimed to investigate the relationship between the Forkhead Box Protein Q1 (FoxQ1) gene and Wnt/β-catenin signaling, and whether this signaling pathway confers resistance to concurrent chemotherapy and radiotherapy in colorectal cancer cells. Further, we also determined whether artemisinin acts on FoxQ1 to reverse this chemoradioresistance by regulating Wnt/β-catenin signaling. We established chemoradioresistant cell (CRR cell) lines HT29/HCT116 in vitro, and cell transfection technology was used to inhibit or overexpress FoxQ1 expression in HT29CRR and HCT116CRR cell lines. After artemisinin treatment, the mRNA and protein expression levels of FoxQ1 and β-catenin were monitored in colorectal cancer cells using RT-qPCR and western blotting, respectively, to verify whether artemisinin can regulate Wnt/β-catenin signaling through FoxQ1. Our results showed that inhibiting FoxQ1 expression in HT29CRR/HCT116CRR cells significantly decreased β-catenin mRNA and protein expression, whereas overexpressing FoxQ1 significantly increased β-catenin expression. Further, the mRNA and protein expression levels of FoxQ1 and β-catenin in artemisinin-treated HT29CRR/HCT116CRR cells were significantly lower than those left untreated. FoxQ1 has a regulatory effect on Wnt/β-catenin signaling during resistance to concurrent chemoradiotherapy. By controlling the Wnt/β-catenin signaling cascade through FoxQ1, artemisinin can reduce the resistance of colorectal cancer to combined chemotherapy and radiotherapy.