Downregulation hsa_circ_0000571 inhibited the malignant progression of NSCLCs by regulation miR-654-5p/S100A11 axis

Accumulation studies confirmed that circRNA play an important role in regulation the progress of non-small cell lung cancer (NSCLC). But the role of circRNA still largely unclear. So, the aim of this study was to explore new circRNA and underlying mechanisms through which they regulate NSCLC progression.

High-throughput sequencing were used to reveal the different expression of circRNA among NSCLC tissues and para-carcinoma tissue. Fluorescence in situ hybridization (FISH) were used to analysis the expression and subcellular localization of hsa_circ_0000571 in both NSCLC tissues and cells line. The regulatory mechanism and targets were then investigated utilizing bioinformatics analyses, luciferase reporter assay, transwell migration, clone formation experiment, CCK8, and EdU analysis. The in vivo experiments was used to elucidate the roles of hsa_circ_0000571 in NSCLC tumor metastasis and growth.

The study found that hsa_circ_0000571 expression was increased in both NSCLC tissues and cell lines, which indicated that hsa_circ_0000571 functions in NSCLC progression. FISH detection also show that hsa_circ_0000571 mainly located in the cytoplasm. And high expression of hsa_circ_0000571 was positively correlated with high tumor grade. Hsa_circ_0000571 downregulation inhibited NSCLC invasion and proliferation in both in vitro as well as in vivo experiments. Luciferase reporter data validated that both miR-654-5p and S100A11 were hsa_circ_0000571 downstream targets. S100A11 overexpression or miR-654-5p inhibition restored NSCLC cell proliferation and invasion post hsa_circ_0000571 silencing. Overexpression S100A11 restored NSCLC cell proliferation and invasion after overexpression miR-654-5p.

Downregulation of hsa_circ_0000571 suppressed NSCLC progression by miR-654-5p/S100A11 axis regulation.