Hsa_circ_0006677 regulates special AT-rich binding protein-2-mediated tumor-suppressive effect via functioning as a miR-1245a sponge in non-small cell lung cancer

Non-small cell lung cancer (NSCLC) is still one of the most challenging malignant tumors. Deregulation of circular RNAs (circRNAs) is associated with NSCLC progression. However, the regulatory mechanism of circRNAs in NSCLC still needs to be studied. We selected a differentially expressed hsa_circ_0006677 (circ_0006677) in NSCLC through analyzing the GSE158695 and GSE112214 datasets. Expression of circ_0006677 was evaluated by real-time quantitative polymerase-chain reaction (RT-qPCR). Effects of circ_0006677 overexpression on NSCLC cell proliferation, apoptosis, migration, invasion, and stemness were determined by clonogenic, 5-ethynyl-2’-deoxyuridine (EdU), flow cytometry, transwell, and sphere formation assays. The regulatory mechanism of circ_0006677 was predicted by bioinformatics analysis and verified by dual-luciferase reporter and RIP assays. Animal experiments were carried out to validate the function of circ_0006677 in vivo. We observed the downregulation of circ_0006677 in NSCLC samples and cells. Functionally, circ_0006677 overexpression decreased xenograft tumor growth and restrained NSCLC cell proliferation, invasion, migration, stemness, and induced NSCLC cell apoptosis in vitro. Molecular mechanism experiments exhibited that circ_0006677 functioned as a miR-1245a sponge and mediated SATB2 expression through adsorbing miR-1245a. Either miR-1245a overexpression or SATB2 knockdown weakened circ_0006677 overexpression-mediated repression on proliferation, invasion, migration, and stemness. In conclusion, circ_0006677 regulated SATB2-mediated tumor-suppressive effect via acting as a miR-1245a sponge in NSCLC, providing a new mechanism for understanding the progression of NSCLC.