Exosomal miR-106a-5p accelerates the progression of nasopharyngeal carcinoma through FBXW7-mediated TRIM24 degradation.

Abstract

Nasopharyngeal carcinoma (NPC) is prevalent in East Asia and causes increased health burden. Elucidating the regulatory mechanism of NPC progression is important for understanding the pathogenesis of NPC and developing novel therapeutic strategies. Nasopharyngeal carcinoma and normal tissues were collected. Nasopharyngeal carcinoma cell proliferation, migration, and invasion were evaluated using CCK‐8, colony formation, wound healing, and transwell assays, respectively. A xenograft mouse model of NPC was established to analyze NPC cell growth and metastasis in vivo. The expression of miR‐106a‐5p, FBXW7, TRIM24, and SRGN was determined with RT‐qPCR and Western blot. MiR‐106a‐5p, TRIM24, and SRGN were upregulated, and FBXW7 was downregulated in NPC tissues and cells. Exosomal miR‐106a‐5p could enter NPC cells, and its overexpression promoted the proliferation, migration, invasion, and metastasis of NPC cells, which were suppressed by knockdown of exosomal miR‐106a‐5p. MiR‐106a‐5p targeted FBXW7 to regulate FBXW7‐mediated degradation of TRIM24. Furthermore, TRIM24 regulated SRGN expression by binding to its promoter in NPC cells. Suppression of exosomal miR‐106a‐5p attenuated NPC growth and metastasis through the FBXW7‐TRIM24‐SRGN axis in vivo. Exosomal miR‐106a‐5p accelerated the progression of NPC through the FBXW7‐TRIM24‐SRGN axis. Our study elucidates novel regulatory mechanisms of NPC progression and provides potential exosome‐based therapeutic strategies for NPC.