Effects of Lidocaine and Ropivacaine on Gastric Cancer Cells Through Down-regulation of ERK1/2 Phosphorylation In Vitro

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...

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Published inAnticancer research Vol. 38; no. 12; pp. 6729 - 6735
Main Authors YANG, WENJING, CAI, JUN, ZHANG, HUIMING, WANG, GUYAN, JIANG, WENGUO
Format Journal Article
LanguageEnglish
Published Greece International Institute of Anticancer Research 01.12.2018
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Abstract 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. 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. 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. 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.
AbstractList 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. 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. 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. 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.
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.
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.BACKGROUNDLidocaine 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.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.MATERIALS AND METHODSAGS 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.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.RESULTSLidocaine (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.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.CONCLUSIONLidocaine 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.
Author WANG, GUYAN
ZHANG, HUIMING
YANG, WENJING
CAI, JUN
JIANG, WENGUO
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Issue 12
Keywords local anaesthetic
ropivacaine
Gastric carcinoma
proliferation
lidocaine
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Snippet Lidocaine and ropivacaine have been widely used in gastric cancer surgery. In recent years, lidocaine and ropivacaine have attracted increasing attention in...
Background: Lidocaine and ropivacaine have been widely used in gastric cancer surgery. In recent years, lidocaine and ropivacaine have attracted increasing...
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StartPage 6729
SubjectTerms Anesthetics
Anesthetics, Local - pharmacology
Apoptosis
Cancer
Cancer therapies
Cell adhesion & migration
Cell cycle
Cell growth
Cell Line, Tumor
Cell migration
Cell proliferation
Down-regulation
Down-Regulation - drug effects
Drug dosages
Electric cells
Extracellular signal-regulated kinase
Gastric cancer
Gentian violet
Humans
Kinases
Lidocaine
Lidocaine - pharmacology
MAP Kinase Signaling System - drug effects
Metastasis
Mitogen-Activated Protein Kinase 1 - metabolism
Mitogen-Activated Protein Kinase 3 - metabolism
Phosphorylation
Phosphorylation - drug effects
Proteins
Ropivacaine
Ropivacaine - pharmacology
Stomach Neoplasms - metabolism
Stomach Neoplasms - pathology
Tumor cell lines
Variance analysis
Title Effects of Lidocaine and Ropivacaine on Gastric Cancer Cells Through Down-regulation of ERK1/2 Phosphorylation In Vitro
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