Numerous studies have discovered that hsa_circ_0063526 (also known as circRANGAP1) is an oncogenic circular RNA (circRNA) in some human tumors, including non-small cell lung cancer (NSCLC). However, the concrete molecular mechanism of circRANGAP1 involved in NSCLC is not completely elucidated. CircRANGAP1, microRNA-653-5p (miR-653-5p), and Type XI collagen (COL11A1) contents were determined via real-time quantitative polymerase chain reaction (RT-qPCR). Cell proliferative ability, migration, and invasion were measured using 5-ethynyl-2 '-deoxyuridine (EdU), colony formation, wound healing, and transwell assays. E-cadherin, N-cadherin, Vimentin, and COL11A1 protein levels were detected via western blot assay. After Starbase software prediction, the binding between miR-653-5p and circRANGAP1 or COL11A1 was verified using a dual-luciferase reporter assay. Besides, the role of circRANGAP1 on tumor cell growth was analyzed using a xenograft tumor model in vivo. Increased circRANGAP1 and COL11A1, and reduced miR-653-5p were found in NSCLC tissues and cell lines. Furthermore, circRANGAP1 absence might hinder NSCLC cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) in vitro. Mechanically, circRANGAP1 functioned as a sponge of miR-653-5p to increase COL11A1 expression. In vivo experiments illustrated that circRANGAP1 knockdown repressed tumor growth. CircRANGAP1 silencing might suppress NSCLC cell malignant biological behaviors, at least in part, through the miR-653-5p/COL11A1 axis. These results provided a promising strategy for treating NSCLC malignancies.