circ-FSCN1 affects ferroptosis and cell viability in NSCLC via the miR-506-3p/SLC7A1 pathway

circRNA is known to have regulatory functions across different cancers. Nevertheless, its regulatory functions in non-small cell lung cancer (NSCLC) are unknown. The present investigation aimed to research circ-FSCN1 expression in NSCLC cells and tissues employing high-throughput sequencing (HTS). NSCLC cells were investigated utilizing the CCK-8, EdU, and Transwell assays. Luciferase reporter assays were employed to verify circ-FSCN1 and its downstream target. Tumorigenesis and metastasis assays were performed to detect the role of circ-FSCN1 in NSCLC. Immunofluorescence was used to detect ROS deposition. The data indicated that the expression of hsa_circ_0004175 (circ-FSCN1) was elevated in NSCLC tissues and cells. The downregulation of circ-FSCN1 inhibited cellular migration and proliferation in the experiments. miR-506-3p downregulation or SLC7A1 overexpression reversed the suppression effects of sh-circ-FSCN1 on the proliferation and migration ability of H1299 and A549 cells. SLC7A1 overexpression reversed the inhibitory effects of miR-506-3p on the proliferation and migration ability of H1299 and A549 cells. The current investigation revealed that inhibiting miR-506-3p or overexpressing SLC7A1 reversed the enhancing effects of sh-circ-FSCN1 on ROS accumulation in H1299 and A549 cells. SLC7A1 overexpression reversed the enhancing effects of miR-506-3p on ROS accumulation in A549 and H1299 cells. Our investigation discovered that circ-FSCN1 affects ferroptosis and cell viability via the miR-506-3p/SLC7A1 pathway in NSCLC. circ-FSCN1 can function as a potential NSCLC diagnostic biomarker and therapy target.