Circ_0058063 Contributed to Oral Squamous Cell Carcinoma Development by Sponging miR-145 and Regulating PI3K/AKT Pathway.

BACKGROUND

Circular RNAs (circRNAs) are key regulators of oral squamous cell carcinoma (OSCC) progression. In this study, we aimed to clarify the regulatory roles of circ_0058063 and its effect on tumorigenesis in OSCC.

METHODS

Quantitative real-time polymerase chain reaction was conducted to determine the expression levels of microRNA (miR)-145-5p and circ_0058063 in OSCC. Cell viability, adhesion, migration, and epithelial-mesenchymal transition (EMT) of OSCC cells were assessed using cell counting kit-8, cell adhesion, and transwell assays. Western blotting was performed to determine the phosphoinositide 3-kinase (PI3K) and protein kinase B (AKT) phosphorylation levels. Xenograft tumor models were constructed to evaluate the tumorigenicity of OSCC cells in vivo. In addition, the interaction between circ_0058063 and miR-145-5p was validated via luciferase reporter and RNA immunoprecipitation assays.

RESULTS

Expression levels of circ_0058063 were elevated, whereas those of miR-145-5p were decreased in OSCC. Upregulation of circ_0058063 levels enhanced the viability, adhesion, migration, and EMT of OSCC cells in vitro and promoted tumorigenicity in vivo. Moreover, circ_0058063 promoted OSCC growth by upregulating the PI3K and AKT phosphorylation levels. miR-145-5p overexpression considerably inhibited the PI3K/AKT pathway and decreased OSCC cell viability, adhesion, migration, and EMT. Mechanistically, circ_0058063 sponged miR-145-5p and activated the PI3K/AKT pathway in OSCC cells.

CONCLUSION

Our results revealed that circ_0058063 functions as an oncogene via regulation of the PI3K/AKT pathway by targeting miR-145-5p in OSCC, suggesting its potential for OSCC diagnosis and treatment.