Upregulation of microRNA-483-5p Advances Non-small Cell Lung Cancer (NSCLC) Progression via Stifling HIPK2 Expression

Abstract

Background: Non-small cell lung cancer (NSCLC) accounts for approximately 80% of lung cancer and has a high incidence and mortality rate. The combination of radiotherapy and chemotherapy is used widely to treat locally advanced NSCLC, but the clinical efficacy is limited. MiRNA-483-5p has been connected to the improvement of an assortment of malignancies. Notwithstanding, its capacity in NSCLC stays obscure. Methods: Here we utilized benefit- or loss-of-miRNA-483-5p expression to investigate the effect of miRNA-483-5p on NSCLC. Results: The results showed that MiRNA-483-5p is entirely up-regulated in NSCLC tissues and cell lines. MiRNA-483-5p inhibitor blocked cell viability, proliferation, migration, invasion but promoted apoptosis, suggesting miRNA-483-5p acts as an oncogene in NSCLC. TargetScan predicted that HIPK2 was an objective gene of miRNA-483-5p. Then, luciferase reporter assay further confirmed that miRNA-483-5p specifically attacked HIPK2’s 3’UTR, suggesting the targeted relationship between miRNA-483-5p and HIPK2. Moreover, HIPK2 acted as a redox signal modulator and was associated with a variety of malignant tumors. The current examination affirmed the low HIPK2 expression in the NSCLC tissues and cell lines. Moreover, overexpression of HIPK2 inhibited NSCLC cell viability, proliferation, migration, invasion, but enhanced apoptosis. More importantly, co-transfection with HIPK2 and miRNA-483-5p reversed these effects, suggesting that miRNA-483-5p facilitated tumor progression by inhibiting HIPK2. Conclusions: Hence, our findings indicated that miRNA-483-5p might be a promising remedial target in NSCLC and give major premise to clinical therapeutics.