Non-small cell lung cancer (NSCLC) is an aggressive malignancy with poor clinical outcomes. Accumulating evidence indicated that dysregulation of circular RNAs (circRNAs) plays a key role in multiple solid tumors. In this study, circ-RAD23B was explored. The expression of circ-RAD23B in NSCLC was detected by RT-qPCR. The clinical value of circ-RAD23B was analyzed by Fisher's exact test and Kaplan-Meier curves. Gain and loss of function experiments were carried out to elucidate the biological functions of circ-RAD23B in NSCLC cell lines. Dual luciferase reporter assay and rescue experiments were used to reveal the mechanism of circ-RAD23B. The findings demonstrated that circ-RAD23B, identified to be amplified and overexpressed in NSCLC, was associated with lymph node invasion, lower differentiation grade and shorter overall survival (OS). Furthermore, circ-RAD23B functions as an oncogene in NSCLC cells. Mechanistically, circ-RAD23B could sponge miR-593-3p and miR-653-5p and thus elevate CCND2 and TIAM1 expression, respectively. Rescue assays proved that circ-RAD23B promotes cell growth via miR-593-3p/CCND2 axis and facilitates cell invasion by miR-653-5p/TIAM1 pathway. Taken together, we propose circ-RAD23B as a promising biomarker and therapeutic target for NSCLC.
Keywords: CCND2; Circ-RAD23B; Non-small cell lung cancer; TIAM1; miR-593–3p; miR-653–5p.
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