CircNTRK2 promotes the progression of nasopharyngeal carcinoma via sponging miR-384 to regulate SOX4 expression

Circular RNAs (circRNAs) have been reported to function critical roles in the pathogenesis and progression of nasopharyngeal carcinoma (NPC). The role of circNTRK2 (circbase ID: hsa_circ_0139142) remains dimness in this disease. This study aimed to investigate the effects and underlying mechanism of circNTRK2 in NPC. GSE143797 was downloaded from the Gene Expression Omnibus (GEO) database, and differently expressed circRNAs were analyzed by the GEO2R method. CircNTRK2 expression was confirmed in human NPC tumor tissues and cell lines by real-time PCR. Loss-of-function studies were used to explore the influence of circNTRK2 on the proliferation, invasion, apoptosis, and epithelial-mesenchymal transition (EMT) of NPC cells. Then, bioinformatic analysis, luciferase reporter assay, biotinylated miRNA pull-down assay, real-time PCR, and Western blotting were applied to clarify the detailed mechanism. We found that circNTRK2 was highly expressed in NPC tissues and cells. Silencing of circNTRK2 inhibited proliferation, invasion and EMT, but facilitated apoptosis of NPC cells in vitro. Also, downregulation of circNTRK2 suppressed tumor growth in a xenograft mouse model. CircNTRK2 directly targeted and negatively mediated miR-384 expression. SOX4 was a target gene of miR-384 in NPC. Both miR-384 inhibitor and SOX4 upregulation could reverse the effects of circNTRK2 knockdown on the proliferation, invasion, EMT, and apoptosis of NPC cells. Whereas miR-384 mimics and SOX4 knockdown abrogated the influences of circNTRK2 upregulation on NPC cells. In conclusion, circNTRK2 promoted NPC progression via sponging miR-384 and inhibiting miR-384 activity, leading to the upregulation of SOX4. This study indicated that circNTRK2 might be a potential target for the treatment of NPC.