Hsa_circ_0016760 exacerbates the malignant development of non-small cell lung cancer by sponging miR-145-5p/FGF5

Hsa_circ_0016760 expression has been reported to be increased in non-small cell lung cancer (NSCLC). The present study was designed to explore the role and mechanism of hsa_circ_0016760 in regulating NSCLC progression. In total, 60NSCLC patients were followed-up for 60 months after surgery. Hsa_circ_0016760 expression in tumor tissues and adjacent non-tumor tissues of NSCLC patients was explored by reverse transcription quantitative polymerase chain reaction (RT-qPCR). NSCLC cell proliferation was monitored by CCK-8 assay and EdU experiment. Transwell assays were used for the detection of NSCLC cell migration and invasion. The target of hsa_circ_0016760 (or miR-145-5p) was validated by luciferase reporter gene assay and RNA immunoprecipitation experiment. A xenograft model was studied with nude mice. Immunohistochemical staining was applied for the detection of Ki67 expression in xenograft tumors. Hsa_circ_0016760/miR-145-5p/FGF5 expression in tissues and cells was investigated by RT-qPCR and western blotting. Hsa_circ_0016760 was aberrantly upregulated in NSCLC, which was associated with poor prognosis of patients (P<0.05). Hsa_circ_0016760 silencing suppressed NSCLC cell proliferation, migration and invasion in vitro (P<0.01). Hsa_circ_0016760 facilitated FGF5 expression via sponging miR-145-5p. The miR-145-5p upregulation or FGF5 downregulation reversed the promoting effect of hsa_circ_0016760 on NSCLC cell proliferation, migration and invasion in vitro (P<0.01). In addition, hsa_circ_0016760 silencing inhibited tumor growth in vivo (P<0.01), and decreased Ki67 expression in xenograft tumors. In conclusion, hsa_circ_0016760 exacerbated the malignant development of NSCLC by sponging miR-145-5p/FGF5.

Automated summary

This study found that Hsa_circ_0016760 exacerbated the malignant development of NSCLC by sponging miR-145-5p to facilitate FGF5 expression. Inhibition of Hsa_circ_0016760 suppressed NSCLC cell proliferation, migration, invasion, and tumor growth, along with decreased Ki67 expression in xenograft tumors.