Conclusion
Hsa_circ_0007637 facilitates NPC progression by sponging miR-636/TPD52 axis.
Methods
Hsa_circ_0007637, miR-636 and TPD52 expressions in 80 NPC patients were detected by quantitative real-time polymerase chain reaction. Hsa_circ_0007637 effect on NPC cell proliferation, apopticosis, invasion and migration was investigated by cell counting kit-8 assay, flow cytometry, transwell experiment and wound healing assay accordingly. Dual-luciferase reporter gene assay, RNA immunoprecipitation experiment and RNA fluorescence in situ hybridization experiment were performed to identify the binding between Hsa_circ_0007637 and miR-636. Dual-luciferase reporter gene assay and RNA pull down assay were conducted to verify the binding between miR-636 and TPD52. TPD52 protein expression in NPC cells was determined by Western blot. In vivo study was performed using nude mice. Immunohistochemistry was performed to assess TPD52 and Ki67 expression in tissues.
Purpose
Hsa_circ_0007637 was discovered to be differentially expressed in nasopharyngeal carcinoma (NPC). However, the exact function and mechanism of Hsa_circ_0007637 on NPC have not been studied. This study firstly researched the function and mechanism of Hsa_circ_0007637 on NPC progression.
Results
Hsa_circ_0007637 was overexpressed in NPC tissues and cells. High Hsa_circ_0007637 expression predicted a poor outcome for NPC patients. Hsa_circ_0007637 knockdown decreased proliferation, invasion, migration and increased apoptosis of NPC cells (P < 0.01). Hsa_circ_0007637 could enhance TPD52 expression via sponging miR-636. miR-636 overexpression or TPD52 knockdown weakened the promoting effect of Hsa_circ_0007637 on NPC cells malignant phenotype (P < 0.01). Hsa_circ_0007637 knockdown suppressed NPC cells growth in vivo (P < 0.01).