FLNA overexpression promotes papillary thyroid cancer aggression via the FAK/AKT signaling pathway.

Abstract

Filamin A (FLNA) is a member of filamin family and has been found to be critical for the progression of several cancers. However, its biological function in papillary thyroid cancer (PTC) remains largely unexplored. Data from The Cancer Genome Atlas (TCGA) databases were utilized to analyze the FLNA expression level and its influence on the clinical implication of patients with PTC. Gene Expression Omnibus (GEO) and quantitative real-time reverse transcriptase PCR (qRT-PCR) was used to verify the expression levels of FLNA in PTC. Kaplan-Meier survival analysis was conducted to evaluate the prognostic value of FLNA in PTC. Transwell assays and wound healing were performed to examine the biological function of FLNA knockdown in PTC cells. Gene set enrichment analysis (GSEA) and Western blotting were conducted to investigate the potential mechanisms underlying the role of FLNA in PTC progression. In addition, the relationship between FLNA expression and tumor immune microenvironment (TME) in PTC was explored. FLNA was significantly upregulated in PTC tissues. High expression level of FLNA was correlated with advanced TNM stage, T stage and N stage, as well as poor disease-free interval (DFI) and progression-free interval (PFI) time in PTC patients. Moreover, we found that FLNA knockdown inhibited the migration and invasion of PTC cells. Mechanistically, FLNA knockdown inhibited epithelial-mesenchymal transition (EMT) in PTC and affected the activation of the FAK/AKT signaling pathway. In addition, FLNA expression was associated with TME in PTC. FLNA may be regarded as a new therapeutic target for PTC patients.