Propofol suppresses non-small cell lung cancer progression by modulating circ_0001727/miR-516b-5p/LRRC1 axis

Background Propofol plays an anti-cancer role in diverse cancers, including non-small cell lung cancer (NSCLC). We aimed to study the function and underlying mechanism of propofol in NSCLC. Methods Cell Counting Kit-8 (CCK-8) and colony formation assays were used to detect cell proliferation. The expression of circ_0001727, microRNA-516b-5p (miR-516b-5p) and leucine-rich repeat-containing protein 1 (LRRC1) mRNA was tested via quantitative real-time polymerase chain reaction (qRT-PCR). Cell migration and invasion were assessed by transwell assay. Angiogenesis and cell apoptosis were determined by tube formation assay and flow cytometry, respectively. Western blot (WB) assay was performed to measure all protein levels. In vivo experiments were conducted via establishing mice xenograft model. Dual-luciferase reporter and RNA Immunoprecipitation (RIP) assays were carried out to verify the relationship between miR-516b-5p and circ_0001727 or LRRC1. Results Circ_0001727 was overexpressed in NSCLC, and propofol treatment reduced circ_0001727 level in NSCLC cells. Propofol could repress proliferation, migration, invasion, and angiogenesis while accelerated apoptosis of NSCLC cells, while these effects were augmented by circ_0001727 knockdown. Moreover, circ_0001727 depletion in combined with propofol also inhibited tumorigenesis in vivo. MiR-516b-5p was targeted by circ_0001727, and miR-516b-5p downregulation counteracted the suppressive influence of circ_0001727 deficiency on the malignant behaviors of NSCLC cells. LRRC1 was targeted by miR-516b-5p, and miR-516b-5p exerted its anti-tumor function in NSCLC cells by targeting LRRC1. Additionally, circ_0001727 regulated LRRC1 expression via sponging miR-516b-5p. Conclusion Propofol inhibited NSCLC progression by regulation of circ_0001727/miR-516b-5p/LRRC1 axis, which might offer an effective therapeutic target for NSCLC therapy.