Abstract
Background
Sinonasal squamous cell carcinoma (SNSCC) is a main subtype of sinonasal malignancy with unclear pathogenesis. microRNAs (miRNAs) are involved in SNSCC progression. Nevertheless, the role and mechanism of miR-362-3p in SNSCC development are unclear.
Methods
The SNSCC tissues (n = 23) and normal sinonasal samples (n = 13) were harvested. SNSCC cell line RPMI-2650 cells were transfected using Lipofectamine 3000. miR-362-3p and pituitary tumor-transforming gene 1 (PTTG1) were determined by quantitative reverse transcription polymerase chain reaction and western blot. Cell proliferation was analyzed via Cell Counting Kit-8 and 5-ethynyl-2′-deoxyuridine assays. Cell migration and invasion was assessed using wound healing assay and transwell assay. Epithelial-mesenchymal transition (EMT)-associated protein (E-cadherin, N-cadherin and Vimentin) levels were measured via western blot. The binding relationship was analyzed via bioinformatic analysis and dual-luciferase reporter assay.
Results
miR-362-3p abundance was decreased in SNSCC samples. miR-362-3p addition constrained cell proliferation, migration, invasion and EMT, but miR-362-3p knockdown played an opposite effect. PTTG1 was targeted and negatively modulated by miR-362-3p. PTTG1 abundance was elevated in SNSCC samples. PTTG1 overexpression mitigated miR-362-3p-modulated suppression of cell proliferation, migration, invasion and EMT in SNSCC cells.
Conclusion
miR-362-3p repressed cell proliferation, migration, invasion and EMT in SNSCC via targeting PTTG1.
Author contributions
JT conceived and designed the experiments, ZLM analyzed and interpreted the results of the experiments, SZ and NL performed the experiments.
Disclosure statement
The authors state that there are no conflicts of interest to disclose.
Data availability statement
All data generated or analyzed during this study are included in this published article.