OBJECTIVE: To probe into the effects of propofol on migration and invasion of cervical cancer cells through miR-802/PTCH1/SHH pathway. METHODS: Human cervical cancer cells HeLa cells were treated with different concentrations of propofol as the propofol group and dimethyl sulfoxide as the control group. MTT and Transwell were used to detect HeLa cell viability

invasion and migration ability. Real-time fluorescent quantitative polymerase chain reaction（RT-qPCR） was used to detect the expression level of miR-802 and PTCH1 mRNA. The target relationship between miR-802 and PTCH1 was verified by bioinformatics analysis and dual luciferase reporter gene system. NC mimic and miR-802 mimic were transfected into HeLa cells and named as NC mimic group and miR-802 mimic group. NC inhibitor

miR-802 inhibitor

Vector

and pcDNA-PTCH1 were transfected into HeLa cells treated with 10 μg/mL propofol and respectively named as propofol+NC inhibitor group

propofol+miR-802 inhibitor group

propofol+Vector group and propofol+pcDNA-PTCH1 group

cell viability

invasion and migration were detected. Western blotting was used to detect the protein expression level of PTCH1 and Gli1. RESULTS: Compared with the control group

the invasion and migration of HeLa cells in the propofol group decreased significantly

with statistically significant difference（P<0.05）. Compared with the NC mimic group

the expression of miR-802 in HeLa cells in miR-802 mimic group increased significantly

and the cell viability

invasion and migration ability decreased

the differences were statistically significant（P<0.05）. Compared with the control group

the expression of miR-802 in HeLa cells in the propofol+NC inhibitor group increased significantly; compared with the propofol+NC inhibitor group

the expression of miR-802 in HeLa cells in the propofol+miR-802 inhibitor group decreased significantly

the cell viability

invasion and migration ability increased

the differences were statistically significant（P<0.05）. PTCH1 was identified as the target gene of miR-802. Compared with the NC inhibitor group

PTCH1 mRNA and protein levels in the miR-802 inhibitor group cells increased significantly

and Gli1 protein expression increased

the differences were statistically significant（P<0.05）. Overexpression of PTCH1 reversed miR-802 and propofol-induced inhibition of HeLa cell viability

migration and invasion ability. CONCLUSIONS: Propofol inhibits the migration and invasion of cervical cancer cells by regulating the miR-802/PTCH1/SHH pathway.