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Lidocaine inhibits melanoma cell proliferation by regulating ERK phosphorylation
Author(s) -
Chen Jun,
Jiao Zhihua,
Wang Aizhong,
Zhong Wenhui
Publication year - 2019
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.27927
Subject(s) - mapk/erk pathway , phosphorylation , lidocaine , melanoma , microbiology and biotechnology , cell growth , cancer research , chemistry , medicine , biology , neuroscience , biochemistry
The melanoma is responsible for the majority of all skin cancer–related deaths worldwide. Evidence suggests that local anesthetics provide some benefit in the treatment of cancer via inhibition of cellular proliferation, invasion and migration. However, the potential antiproliferative effects of local anesthetics in the treatment of melanoma remain to be elucidated. In this study, we investigated the antiproliferative effects and underlying mechanism of the commonly used local anesthetic (lidocaine) on melanoma cells. A375 melanoma cells were treated by lidocaine or vemurafenib. Cell Counting Kit‐8, histological staining, flow cytometric analysis, immunohistochemical staining, and Western blot analyses were carried out to test the effects of lidocaine and vemurafenib on A375 cells. BALB/C‐nu/nu mice intraperitoneally injected with A375 cells were treated by lidocaine, and then tumor volume and weight were calculated. Lidocaine exhibited vemurafenib‐like effects totally. Lidocaine inhibited A375 melanoma cell proliferation in a dose‐ and time‐dependent manner and colony formation also showed a dose‐dependent inhibition. Lidocaine treatment resulted in the arrest of cell‐cycle progression in the G1 phase and inhibited Ki‐67 expression in a dose‐dependent manner. This effect was associated with inhibited extracellular signal–regulated kinase (ERK) phosphorylation. In vivo experiments revealed that intravenous injections of lidocaine suppressed tumor volume and weight. Lidocaine inhibits melanoma cell proliferation in a dose‐ and time‐dependent manner via a mechanism that may involve inhibition of the ERK signaling pathway. Thus, lidocaine may provide some benefit for the treatment of melanoma.

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