CircMIIP Contributes to Non-Small Cell Lung Cancer Progression by Binding miR-766-5p to Upregulate FAM83A Expression.

BACKGROUND

Circular RNA migration and invasion inhibitory protein (circMIIP) is reported to be upregulated in non-small cell lung cancer (NSCLC) tissues compared with normal tissues. However, the role and working mechanism of circMIIP in NSCLC progression remain largely unclear.

METHODS

Cell proliferation ability was analyzed by colony formation assay, cell counting kit-8 (CCK-8) assay, and 5-ethynyl-2'-deoxyuridine assay. Cell apoptosis was assessed by flow cytometry. Transwell assays were performed to analyze the migration and invasion abilities of NSCLC cells. The interaction between microRNA-766-5p (miR-766-5p) and circMIIP or family with sequence similarity 83A (FAM83A) was validated by dual-luciferase reporter assay and RNA immunoprecipitation assay. Xenograft tumor model was established to analyze the role of circMIIP on tumor growth in vivo.

RESULTS

CircMIIP was highly expressed in NSCLC tissues and cell lines. CircMIIP knockdown restrained the proliferation, migration and invasion and induced the apoptosis of NSCLC cells. CircMIIP acted as a molecular sponge for miR-766-5p, and circMIIP silencing-mediated anti-tumor effects were largely overturned by the knockdown of miR-766-5p in NSCLC cells. miR-766-5p interacted with the 3' untranslated region (3'UTR) of FAM83A, and FAM83A overexpression largely reversed miR-766-5p accumulation-induced anti-tumor effects in NSCLC cells. CircMIIP competitively bound to miR-766-5p to elevate the expression of FAM83A in NSCLC cells. CircMIIP knockdown significantly restrained xenograft tumor growth in vivo.

CONCLUSION

CircMIIP promoted cell proliferation, migration and invasion and suppressed cell apoptosis in NSCLC cells through mediating miR-766-5p/FAM83A axis.