FOLR1-stabilized β-catenin promotes laryngeal carcinoma progression through EGFR/AKT/GSK-3β pathway.

Folate receptor 1 (FOLR1) is overexpressed in numerous epithelial malignancies; however, its role in laryngeal squamous cell carcinoma (LSCC) remains unclear. In the present study, we demonstrated that FOLR1 messenger RNA and protein expression levels were higher in LSCC tissues than in the adjacent normal tissues. Additionally, FOLR1 promoted the proliferation and migration of LSCC cells, whereas small interfering RNA-mediated knockdown of β-catenin abolished these effects. Moreover, FOLR1 stabilizes β-catenin by inhibiting its ubiquitination and degradation. Furthermore, blocking the interaction between epidermal growth factor receptor (EGFR) and the EGFR/AKT/glycogen synthase (GSK)3β signaling axis both abolished FOLR1's effects on the expression and nuclear aggregation of β-catenin. In summary, our work reveals a novel mode in which FOLR1 promotes the proliferation and migration of LSCC by enhancing the stability and nuclear translocation of β-catenin through the EGFR/AKT/GSK3β axis. © 2023 Wiley Periodicals LLC.

Citation

Huawei Tuo, Xuemei Li, Haixia Du, Man Li, Chenli Xu, Zizhong Yu, Huzi Zhao. FOLR1-stabilized β-catenin promotes laryngeal carcinoma progression through EGFR/AKT/GSK-3β pathway. Molecular carcinogenesis. 2023 Sep 13

PMID: 37702010

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