Silencing KPNA2 Promotes Ferroptosis in Laryngeal Cancer by Activating the FoxO Signaling Pathway Silencing KPNA2 Promotes Ferroptosis in LAC

Author:

Xu Mimi1,Hu Xiaoqi1,Xiao Zhixue1,Zhang Siyi1,Lu Zhongming1

Affiliation:

1. Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Southern Medical University

Abstract

AbstractObjective Ferroptosis induction is a novel approach to oncotherapy, with few studies in laryngeal cancer. This article is forward to providing a new ferroptosis-related biomarker for laryngeal cancer. Methods We downloaded the microarray datasets GSE127165 and GSE51985 from the Gene Expression Omnibus database and obtained the differentially expressed genes (DEGs) associated with ferroptosis. The Hub genes were identified after the construction of the protein-protein interaction network and verified by principal component analysis. KPNA2 was selected and verified by Receiver operating characteristic curve and pan-cancer analysis. Then we conducted experimental verification by silencing KPNA2 in ferroptosis-induced laryngeal cancer cells by Erastin. Results 45 DEGs associated with ferroptosis in laryngeal cancer were obtained, and KPNA2 of 5 hub genes with high degrees in the protein-protein interaction network was further selected, which showed a high expression in pan-cancer including laryngeal cancer, considerable diagnostic efficiency, and a correlation with tumor prognosis and immune infiltration. In ferroptosis-induced laryngeal cancer cells, we found an increased expression of cyclooxygenase 2, iron ions, and malondialdehyde, and a decreased expression of glutathione peroxidase 4 and glutathione when the expression of KPNA2 was suppressed. The FoxO signaling pathway in laryngeal cancer cells was activated by silencing KPNA2. Conclusion KPNA2 is possibly a promising therapeutic target for laryngeal cancer, which can suppress ferroptosis in laryngeal cancer by inhibiting the FoxO signaling pathway.

Publisher

Research Square Platform LLC

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