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Abstract
Application for ESRA Abstract Prizes: I apply as an Anesthesiologist (Aged 35 years old or less)
Background and Aims Retrospective and clinical studies on patient undergoing cancer surgery suggested the perioperative use of local anesthetic drugs might improve the outcome. Previous publications indicated that lidocaine reduced cancer metastasis by inhibiting the tyrosine kinase enzyme Src. However, there is no data investigating the impact of lidocaine in non-epithelial cancer cells. The aim of this investigation was to explore in vitro the impact of lidocaine on cancer of mesenchymal origin. For this purpose, osteosarcoma and Ewing sarcoma cell lines were used.
Methods Adhesion assays were performed by treating the cells for 48h compared to verteporfin in 6 well plates. Migration was assessed by the Boyden chamber migration during 48h. DMSO was used as control. Wound healing assays was performed during 48h and assessed with the MRI wound healing tool in Image J in cells being treated either with or without TNF-α. Src activity was evaluated by western blotting.
Results Adhesion (figure 1), migration (figure 2) and wound healing (figure 3) were not influenced by the presence of lidocaine with or without stimulation with TNF- α. The addition of methylnaltrexone did not modify the results. Src activity was similar to the control and not increased by the addition of TNF- α.
Adhesion
Migration
Wound healing
Conclusions Contrary to what has been found with cancer originating from epithelial cells, lidocaine does not prevent adhesion and migration of osteosarcoma and Ewing sarcoma cells from mesenchymal origin. Further investigations, including Src pathway activation, would be required to identify mechanistic differences between cells of epithelial or mesenchymal origin towards anti-metastatic properties of local anesthetics.