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Lidocaine inhibits cytoskeletal remodelling and human breast cancer cell migration.
背景與目的
乳腺癌細(xì)胞的轉(zhuǎn)移潛能與趨化因子CXCL12的過(guò)表達(dá)和其受體CXCR4的活性密切相關(guān)。利多卡因是一種可在乳腺癌切除術(shù)中使用的局部麻醉劑，可抑制癌細(xì)胞的生長(zhǎng)、侵襲和遷移。因此，我們?cè)谌橄侔┘?xì)胞系中研究了利多卡因是否可以調(diào)節(jié)CXCL12誘導(dǎo)的反應(yīng)。
方 法
在暴露于利多卡因（10μM或100μM）后，以人乳腺癌上皮細(xì)胞系MDA-MB-231細(xì)胞在體外評(píng)估細(xì)胞內(nèi)鈣水平、細(xì)胞骨架重塑和細(xì)胞遷移。
結(jié) 果
利多卡因（10或100μM）顯著抑制CXCR4信號(hào)傳導(dǎo)，導(dǎo)致鈣釋放減少（Fluo 340 nm / 380 nm，平均差異0.76，p <0.0001），細(xì)胞骨架重塑受損和趨化性實(shí)驗(yàn)（熒光平均強(qiáng)度，0.16，P = 0.0047）中，癌細(xì)胞的活動(dòng)性均降低。 利多卡因的作用與CD44粘附分子的調(diào)節(jié)無(wú)關(guān)。
結(jié) 論
在臨床濃度下，利多卡因顯著抑制CXCR4信號(hào)傳導(dǎo)。我們所提出的結(jié)果為控制利多卡因?qū)?xì)胞遷移的抑制作用的分子機(jī)制提供了新的見(jiàn)解。
原始文獻(xiàn)摘要
G. D’Agostino1, A. Saporito2, V. Cecchinato1 , et al. Lidocaine inhibits cytoskeletal remodelling and human breast cancer cell migration.[B]. British Journal of Anaesthesia,1e7 (2018) ,doi: 10.1016/j.bja.2018.07.015
Abstract Background: The metastatic potential of breast cancer cells has been strongly associated with overexpression of the chemokine CXCL12 and the activity of its receptor CXCR4. Lidocaine, a local anaesthetic that can be used during breast cancer excision, inhibits the growth, invasion, and migration of cancer cells. We therefore investigated, in a breast cancer cell line, whether lidocaine can modulate CXCL12-induced responses. Methods: Intracellular calcium, cytoskeleton remodelling, and cell migration were assessed in vitro in MDA-MB-231 cells, a human breast cancer epithelial cell line, after exposure to lidocaine (10 mM or 100 mM). Results: Lidocaine (10 or 100 mM) significantly inhibited CXCR4 signalling , resulting in reduced calcium release (Fluo 340 nm/380 nm, 0.76 mean difference, p<0.0001), impaired cytoskeleton remodelling (F-Actin fluorescence mean intensity, 21 mean difference, P?0.002), and decreased motility of cancer cells, both in the scratch wound assay (wound area at 21 h, 19%, P<0.0001), and in chemotaxis experiments (fluorescence mean intensity, 0.16, P?0.0047). The effect of lidocaine was not associated with modulation of the CD44 adhesion molecule. Conclusions: At clinical concentrations, lidocaine significantly inhibits CXCR4 signalling. The results presented shed new insights on the molecular mechanisms governing the inhibitory effect of lidocaine on cell migration.
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