Lei Zhang1, Rong Hu1, Yanyong Cheng1, Xiaoyang Wu1, Siwei Xi1, Yu Sun1, Hong Jiang1. 1. Department of Anesthesiology, Shanghai Ninth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Center for Specialty Strategy Research of Shanghai Jiao Tong University China Hospital Development Institute, Shanghai, China.
Abstract
OBJECTIVES: Lidocaine is the most commonly used local anaesthetic in clinical and can inhibit proliferation, suppress invasion and migration and induce apoptosis in human lung adenocarcinoma (LAD) cells. However, its specific downstream molecular mechanism is unclear. MATERIALS AND METHODS: LAD cell lines, A549 and H1299 cells, were treated with lidocaine. The proliferation was evaluated by the methylthiazolyldiphenyl-tetrazolium bromide (MTT) and bromodeoxyuridine (BrdU) assay. The expression level of related proteins was detected by real-time quantitative PCR (qPCR) and Western blot assay. RESULTS: The results indicated that lidocaine dose-dependently suppressed the proliferation of A549 and H1299 cells. In the LAD patients' samples, GOLT1A was upregulated and involved in the poor prognosis and higher grade malignancy. Additionally, GOLT1A mediates the function of lidocaine on repressing proliferation by regulating the cell cycle in A549 cells. CONCLUSIONS: Our findings suggest that lidocaine downregulates the GOLT1A expression to repress the proliferation of lung cancer cells.
OBJECTIVES:Lidocaine is the most commonly used local anaesthetic in clinical and can inhibit proliferation, suppress invasion and migration and induce apoptosis in humanlung adenocarcinoma (LAD) cells. However, its specific downstream molecular mechanism is unclear. MATERIALS AND METHODS:LAD cell lines, A549 and H1299 cells, were treated with lidocaine. The proliferation was evaluated by the methylthiazolyldiphenyl-tetrazolium bromide (MTT) and bromodeoxyuridine (BrdU) assay. The expression level of related proteins was detected by real-time quantitative PCR (qPCR) and Western blot assay. RESULTS: The results indicated that lidocaine dose-dependently suppressed the proliferation of A549 and H1299 cells. In the LADpatients' samples, GOLT1A was upregulated and involved in the poor prognosis and higher grade malignancy. Additionally, GOLT1A mediates the function of lidocaine on repressing proliferation by regulating the cell cycle in A549 cells. CONCLUSIONS: Our findings suggest that lidocaine downregulates the GOLT1A expression to repress the proliferation of lung cancer cells.
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