Skip to main content
. 2022 Jul 14;22:765. doi: 10.1186/s12885-022-09848-y

Fig. 5.

Fig. 5

Propofol upregulated miR-486-5p to inactivate the RAP1-NF-κB pathway in NSCLC. a The potential target sites between miR-486-5p and 3’UTR of the RAP1 gene was predicted on the online starbase website. b The wild-type RAP1 and mutant RAP1 were separately transfected to HEK-293 cells along with NC mimic or miR-486 mimic, and then the targeting relationship between miR-486-5p and RAP1 gene was verified by dual luciferase reporter assay. qRT-PCR(c) and western blot (d-e) were performed to detect the expression of the RAP1/NF-κB axis in cells with miR-486-5p overexpression or knockdown. f The expression of the RAP1/NF-κB axis in DDP-resistant cells treated with miR-486-5p inhibitor, propofol and DDP. g The expression of nuclear NF-κB p65 and cytoplasmic NF-κB p65 in DDP-resistant cells treated with miR-486-5p inhibitor, propofol and DDP. *P < 0.05. NC mi, negative control mimic. miR mi, miR-486-5p mimic. NC in, negative control inhibitor. miR in, miR-486-5p inhibitor. NC, control. Ppf, high concentration of propofol. miR in, miR-486-5p inhibitor