Conclusions
MiR-103 might play a key role in NPC carcinogenesis by targeting TIMP-3 and affecting the Wnt/β-catenin pathway. Level of evidence: NA Laryngoscope, 130:E75-E82, 2020.
Methods
Tissue inhibitor of metalloproteinases-3 (TIMP-3) was identified as the theoretical target gene of miR-103, and its regulatory mechanism in NPC was explored by quantitative reverse transcription polymerase chain reaction, Western blot, MTT, transwell, and luciferase reporter assays.
Results
MiR-103 was upregulated whereas TIMP-3 was markedly decreased in NPC tissue samples. Ectopic expression of miR-103 promoted NPC cell viability, migration, and invasion. In vitro assay showed that TIMP-3 recovered miR-103-mediated promotion of NPC cell viability, migration, and invasion. The expression of Wnt/β-catenin pathway markers (β-catenin and cyclin D1) were enhanced after miR-103 overexpression. Conclusions: MiR-103 might play a key role in NPC carcinogenesis by targeting TIMP-3 and affecting the Wnt/β-catenin pathway. Level of evidence: NA Laryngoscope, 130:E75-E82, 2020.