Abstract

This study investigated the effects of propofol on gastric cancer MKN45 cell proliferation, migration, invasion and apoptosis, as well as underlying potential mechanisms. 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. 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. 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.

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