Abstract
Anaplastic thyroid cancer (ATC) is a rare thyroid tumor associated with high mortality rates; thus, the identification of novel molecular targets and the development of therapeutic strategies are urgently required. The present study aimed to investigate the role of SRY‑related HMG box‑2 (SOX2) in ATC cells and explore whether the underlying mechanism was associated with fibronectin 1 (FN1). The proliferative, migratory and invasive ability of ATC cell lines was investigated using Cell Counting Kit‑8, colony formation, wound‑healing and Transwell assays, respectively; SOX2 expression in FRO cells was knocked down using small interfering RNA and SOX2 overexpression in FRO cells was achieved using cDNA constructs; and reverse transcription‑quantitative PCR and western blotting were used to identify the mechanism of action underlying the SOX‑2 mediated increased in cell aggressive phenotypes. Increased protein expression levels of SOX2 protein were observed in ATC tissue, and FRO and 8505c ATC cell lines. SOX2 overexpression increased the cell viability, and proliferative, migratory and invasive abilities of FRO cell lines. SOX2 overexpression increased FN1, p65, phosphorylated PI3K and AKT expression levels, whereas the knockdown of SOX2 promoted the opposite effects. In conclusion, the present study suggested a possible model of SOX2‑mediated gene regulation in ATC cells, in which the overexpression of SOX2 promoted FN1 expression via the PI3K/AKT signaling pathway to induce the aggressive phenotype of ATC. These findings may provide crucial molecular insights into ATC pathogenesis and may demonstrate potential to develop into novel therapeutic interventions for patients with ATC.