Wenjing Yang1,2, Jun Cai2, Huiming Zhang3, Guyan Wang1, Wenguo Jiang4. 1. Department of Anesthesiology, Beijing Tong Ren Hospital, Capital Medical University, Beijing, P.R. China. 2. Cardiff China Medical Research Collaborative, Cardiff University-Peking University Joint Cancer Institute, Henry Wellcome Building, School of Medicine, Cardiff University, Cardiff, U.K. 3. Department of General Surgery, Beijing Friendship Hospital Affiliated to Capital Medical University, Beijing, P.R. China. 4. Cardiff China Medical Research Collaborative, Cardiff University-Peking University Joint Cancer Institute, Henry Wellcome Building, School of Medicine, Cardiff University, Cardiff, U.K. jiangw@cardiff.ac.uk.
Abstract
BACKGROUND: Lidocaine and ropivacaine have been widely used in gastric cancer surgery. In recent years, lidocaine and ropivacaine have attracted increasing attention in cancer research, whilst effects of lidocaine and ropivacaine on gastric cancer cells have not been investigated before. This study explored the effect of lidocaine and ropivacaine on AGS and HGC-27 gastric cancer cells. MATERIALS AND METHODS: AGS and HGC-27 cells were incubated with lidocaine or ropivacaine at concentrations of 10, 100 and 1 mM. At 24, 48 and 72 h after treatment, proliferation and invasion were evaluated by crystal violet assay and transwell invasion assay. Electric cell-substrate impedance sensing was applied to measure the migration of cancer cells. Phosphorylation status of extracellular-regulated protein kinases (ERK1/2) was evaluated by western blot analysis. RESULTS: Lidocaine (1 mM) and ropivacaine (1 mM) significantly inhibited the proliferation of AGS and HG-27 cells, but had no significant effects on invasion. Lidocaine (1 mM) and ropivacaine (1 mM) also inhibited the migration of AGS and HGC-27cells. After treatment with lidocaine (1 mM) or ropivacaine (1 mM) for 24 h, the phosphorylation of ERK1/2 in AGS and HGC-27 cells was reduced. CONCLUSION: Lidocaine at a clinically relevant concentration (10 μM), and ropivacaine at 1 mM inhibited the proliferation of gastric cancer cell lines by down-regulation of p-ERK1/2. The migration of HGC-27 cells, rather than AGS cells was more obviously inhibited by lidocaine (1 mM) and ropivacaine (1 mM). This research is easy to implement, and lays a foundation for the future research of local anaesthetics in cancer. Copyright
BACKGROUND:Lidocaine and ropivacaine have been widely used in gastric cancer surgery. In recent years, lidocaine and ropivacaine have attracted increasing attention in cancer research, whilst effects of lidocaine and ropivacaine on gastric cancer cells have not been investigated before. This study explored the effect of lidocaine and ropivacaine on AGS and HGC-27 gastric cancer cells. MATERIALS AND METHODS:AGS and HGC-27 cells were incubated with lidocaine or ropivacaine at concentrations of 10, 100 and 1 mM. At 24, 48 and 72 h after treatment, proliferation and invasion were evaluated by crystal violet assay and transwell invasion assay. Electric cell-substrate impedance sensing was applied to measure the migration of cancer cells. Phosphorylation status of extracellular-regulated protein kinases (ERK1/2) was evaluated by western blot analysis. RESULTS:Lidocaine (1 mM) and ropivacaine (1 mM) significantly inhibited the proliferation of AGS and HG-27 cells, but had no significant effects on invasion. Lidocaine (1 mM) and ropivacaine (1 mM) also inhibited the migration of AGS and HGC-27cells. After treatment with lidocaine (1 mM) or ropivacaine (1 mM) for 24 h, the phosphorylation of ERK1/2 in AGS and HGC-27 cells was reduced. CONCLUSION:Lidocaine at a clinically relevant concentration (10 μM), and ropivacaine at 1 mM inhibited the proliferation of gastric cancer cell lines by down-regulation of p-ERK1/2. The migration of HGC-27 cells, rather than AGS cells was more obviously inhibited by lidocaine (1 mM) and ropivacaine (1 mM). This research is easy to implement, and lays a foundation for the future research of local anaesthetics in cancer. Copyright