Purpose: This study investigated the effects of propofol on gastric cancer MKN45 cell proliferation, migration, invasion and apoptosis, as well as underlying potential mechanisms.
Methods: The viability, proliferation, apoptosis, migration and invasion of MKN45 cells were assessed using CCK-8 assay, BrdU incorporation assay, Annexin V-FITC/PI staining, two-chamber migration (invasion) assay and western blotting, respectively. qRT-PCR was performed to measure the expression of microRNA-195 (miR-195). Cell transfection was conducted to down-regulate the expression of miR-195.
Results: Propofol treatment suppressed MKN45 cell proliferation, migration and invasion, but promoted cell apoptosis. The expression of miR-195 was increased after propofol treatment. Suppression of miR-195 reversed the propofol-induced MKN45 cell proliferation, migration and invasion inhibition, as well as apoptosis. Moreover, Propofol treatment inactivated JAK/STAT and NF-κB pathways in MKN45 cells. Suppression of miR-195 reversed the propofol-induced inactivation of JAK/STAT and NF-κB pathways. Inhibition of JAK/STAT and NF-κB pathways reversed the effects of miR-195 suppression on propofol-induced MKN 45 cell proliferation, migration and invasion inhibition, as well as apoptosis enhancement.
Conclusion: Propofol inhibited proliferation, migration and invasion of gastric cancer MKN45 cells by up-regulating miR-195 and then inactivating JAK/STAT and NF-κB pathways. Propofol could be as an effective therapeutic medicine for gastric cancer treatment.
Keywords: Gastric cancer; MicroRNA-195; Propofol.
Copyright © 2018. Published by Elsevier B.V.