Objective: To detect the effect of brain cytoplasmic RNA 1 (BCYRN1) on the proliferation and migration of airway smooth muscle cells (ASMCs) in rat model of asthma. Methods: Male SD rats were randomly divided into control group and asthma group (n=10 each). The ovalbumin (OVA) model was constructed in asthma group. Real time-qPCR was performed to detect the level of BCYRN1 in the ASMCs separated from the airway tissue of these rats. Then 2-(4-iodophenyl)-3-(4-nitrophenyl)-5-(2, 4-disulfophenyl)-2H-tetrazolium (WST-1) assay, roche real-time cell analyzer assay and Transwell cell migration assay were performed to detect the viability/proliferation and migration of ASMCs which were transfected with Ad-BCYRN1.Platelet-derived growth factor (PDGF)-BB was used to treat ASMCs to induce proliferation and migration, and the level of BCYRN1 was examined.The viability/proliferation and migration of ASMCs treated with PDGF-BB and transfected with si-BCYRN1 were detected. Inspiratory resistance and expiratory resistance were measured in rats with BCYRN1 knockdown.Briefly, rats were randomly divided into four groups: control (group A), sensitization + Ad-GFP (group B), sensitization + AdSM22α-siBCYRN1 (group C), control + Ad-SM22α-siBCYRN1 (group D) (n=10 each). The corresponding adenovirus vectors were sent to lung of group B, group C and group D through nasal spray. The OVA model was constructed in group B and group C. The rats in group A and group D were treated with saline.After 24 h of the last treatment with OVA or saline, rats of each group were given tracheal intubation, connected with breathing machine. Rats were injected with methacholine to measure the inspiratory resistance and expiratory resistance. Results: The level of BCYRN1 in ASMCs separated from rats in asthma group and in ASMCs treated with PDGF-BB was 3.60±0.45 and 3.53±0.35, respectively, significantly higher than those of the corresponding control (both P<0.01). Ad-BCYRN1 significantly increased the expression of BCYRN1 in ASMCs. The cell viability and proliferation rates of ASMCs transfected with Ad-BCYRN1 increased 1.75-and 1.47-fold compared to those of the control group, respectively (P<0.01); mobility increased 2.42-fold compared to that of the control group (all P<0.01). BCYRN1 knockdown reversed the increasing proliferation and migration of ASMCs induced by PDGF-BB. The cell proliferation rate and cell migration number in the PDGF-BB treatment group were (4.87±0.21)% and 80.00±5.00, respectively, which were significant higher than those in the si-BCYRN1 transfected group ((3.63±0.21)% and 25.33±2.52, all P<0.01). BCYRN1 knockdown reduced the inspiratory resistance and expiratory resistance in sensitization + Ad-SM22α-siBCYRN1 group. When the concentration of acetylcholine reached 1 mg/kg, the inspiratory resistance in the group A, group B, group C, and group D were 8.27±0.21, 25.40±0.56, 12.07±0.67 and 8.40±0.46 cmH2O·s·ml-1, and expiratory resistance were 13.30±0.56, 38.37±1.33, 16.40±0.56 and 13.40±0.46 cmH2O·s·ml-1, respectively (all P<0.01). Conclusion: Overexpression of BCYRN1 promotes the proliferation and migration of ASMCs in rat model of asthma.