LAUSR

AIMS Circular RNAs (circRNAs) are relevant to atherosclerosis progression. However, the role and mechanism of circRNA hsa_circ_0029589 (circ_0029589) in atherosclerosis are not fully understood. This research aims to explore the function and mechanism of circ_0029589 in oxidized low-density lipoprotein (ox-LDL)-caused vascular smooth muscle cells (VSMCs) injury in vitro. MAIN METHODS VSMCs were challenged via ox-LDL to mimic atherosclerosis-like injury in vitro. Circ_0029589, microRNA-214-3p (miR-214-3p) and stromal interaction molecule 1 (STIM1) abundances were detected via quantitative reverse transcription polymerase chain reaction or western blot. Cell proliferation was investigated via cell viability, cycle, apoptosis and proliferation-associated protein levels. Cell migration and invasion were assessed via transwell analysis. The relationship between miR-214-3p and circ_0029589 or STIM1 was tested via dual-luciferase reporter analysis and RNA immunoprecipitation. KEY FINDINGS Circ_0029589 level was enhanced in ox-LDL-challenged VSMCs. Circ_0029589 interference constrained cell proliferation, migration and invasion in ox-LDL-challenged VSMCs. miR-214-3p was targeted by circ_0029589 and miR-214-3p knockdown weakened the suppressive function of circ_0029589 silence on VSMCs proliferation, migration and invasion. STIM1 was targeted via miR-214-3p and miR-214-3p could suppress VSMCs proliferation, migration and invasion via decreasing STIM1. Moreover, circ_0029589 modulated STIM1 level by miR-214-3p. SIGNIFICANCE Circ_0029589 knockdown repressed proliferation, migration and invasion of VSMCs challenged via ox-LDL by regulating miR-214-3p and STIM1, indicating that circ_0029589 might play important role in atherosclerosis.