Wenyu Zhang1, Yang Wang2, Zhihua Zhu1, Yan Zheng1, Bin Song3. 1. Department of Anesthesiology, China-Japan Union Hospital of Jilin University, Changchun 130033, Jilin, China. 2. Department of Orthopaedics, China-Japan Union Hospital of Jilin University, Changchun 130033, Jilin, China. 3. Department of Gastrointestinal Colorectal and Anal Surgery, China-Japan Union Hospital of Jilin University, Changchun 130033, Jilin, China. Electronic address: songb312@sina.com.
Abstract
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.
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.