Objective To investigate the effect of butorphanol on the malignant biological behavior of glioma cells by regulating the sonic hedgehog (SHH)/glioma-associated oncogene homolog 1 (GLI1) signaling pathway.

Methods Glioma LN229 cells were divided into control group, low-dose butorphanol group, medium-dose butorphanol group, high-dose butorphanol group, high-dose butorphanol+pcDNA3.1 group and high-dose butorphanol+pc-SHH group. MTT and Edu assays were used to detect cell proliferation; flow cytometry was used to detect cell apoptosis rate; Transwell chamber assay was used to detect cell migration and invasion; real-time fluorescent quantitative polymerase chain reaction (qRT-PCR) was used to detect SHH mRNA and GLI1 mRNA expression levels; Western blot was used to detect the protein expression levels of Ki-67, matrix metalloproteinase-2 (MMP-2), cleaved caspase-3, SHH and GLI1.

Results Butorphanol could reduce the viability and proliferation rate of LN229 cells, and decreased the number of cell migration and invasion (P < 0.05). Butorphanol could reduce the expression levels of SHH mRNA, GLI1 mRNA and the protein expression of Ki-67, MMP-2, SHH as well as GLI1 in LN229 cells, promote cell apoptosis and increase the protein expression of cleaved caspase-3 (P < 0.05). Overexpression of SHH could partially reverse the inhibitory effect of butorphanol on LN229 cells (P < 0.05).

Conclusion Butorphanol can inhibit the malignant biological behavior of glioma cells, and its mechanism may be related to the inhibition of the SHH/GLI1 signaling pathway.