Objectives/Hypothesis
To verify how microRNA‐103 (miR‐103) is involved in nasopharyngeal carcinoma (NPC) development.
Study Design
Research on the relationship between miR‐103 and NPC.
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