Abstract
Accumulating evidence suggests that circular RNAs (circRNAs) play important regulatory roles in non-small cell lung cancer (NSCLC). At present, we aimed to explore the regulatory role of has_circ_0003528 (circ_0003528) in NSCLC. Alterations of circ_0003528 expression in NSCLC samples and cell lines were detected by real-time quantitative polymerase chain reaction (RT-qPCR). Impacts of circ_0003528 on NSCLC cell malignant transformation were analyzed by 3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium Bromide (MTT), 5-ethynyl-2'-deoxyuridine (EdU), flow cytometry, transwell invasion, and tube formation assays. Epithelial-mesenchymal transition (EMT)-related markers were detected with western blotting. Pro-inflammatory cytokines were detected by Enzyme-linked immunosorbent assay (ELISA). The regulation mechanism of circ_0003528 was verified by dual-luciferase reporter and RNA pull-down assays. The tumorigenesis role of circ_0003528 was verified by animal experiments. Higher levels of circ_0003528 were obtained in NSCLC samples and cell lines, and patients with high circ_0003528 expression had a worse prognosis. Silence of circ_0003528 decreased xenograft growth in mouse models and induced cell apoptosis and repressed cell viability, proliferation, invasion, EMT, angiogenesis, and immune escape in NSCLC cells in vitro. Mechanistically, circ_0003528 controlled programmed cell death ligand 1 (PDL1) expression through interaction with miR-511-3p. The inhibiting impacts of circ_0003528 knockdown on NSCLC cell malignant transformation and immune escape were weakened after miR-511-3p silencing. Moreover, PDL1 overexpression partially counteracted miR-511-3p upregulation-mediated suppression on NSCLC cell malignant transformation and immune escape. Circ_0003528 facilitated NSCLC cell malignant transformation and immune escape through regulation of the miR-511-3p/PDL1 axis, highlighting the oncogenic role of circ_0003528 in NSCLC.
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