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高浓度的维生素C会诱导恶性黑色素瘤产生细胞毒性,但低浓度时会促进肿瘤生长。

Vitamin C at high concentrations induces cytotoxicity in malignant melanoma but promotes tumor growth at low concentrations.

作者信息

Yang Guang, Yan Yao, Ma Younan, Yang Yixin

机构信息

Department of Biological Sciences, Emporia State University, Emporia, Kansas.

出版信息

Mol Carcinog. 2017 Aug;56(8):1965-1976. doi: 10.1002/mc.22654. Epub 2017 Apr 24.

Abstract

Vitamin C has been used in complementary and alternative medicine for cancers regardless of its ineffectiveness in clinical trials and the paradoxical effects antioxidants have on cancer. Vitamin C was found to induce cytotoxicity against cancers. However, the mechanisms of action have not been fully elucidated, and the effects of vitamin C on human malignant melanoma have not been examined. This study revealed that vitamin C at millimolar concentrations significantly reduced the cell viability as well as invasiveness, and induced apoptosis in human malignant melanoma cells. Vitamin C displayed stronger cytotoxicity against the Vemurafenib-resistance cell line A2058 compared with SK-MEL-28. In contrast, vitamin C at micromolar concentrations promoted cell growth, migration and cell cycle progression, and protected against mitochondrial stress. Vemurafenib paradoxically activated the RAS-RAF-MEK-ERK signaling pathway in the Vemurafenib-resistant A2058, however, vitamin C abolished the activations. Vitamin C displayed synergistic cytotoxicity with Vemurafenib against the Vemurafenib-resistant A2058. In vivo assay suggested that lower dosage (equivalent to 0.5 g/70 kg) of vitamin C administered orally increased the melanoma growth. Therefore, vitamin C may exert pro- or anti-melanoma effect depending on concentration. The combination of vitamin C at high dosage and Vemurafenib is promising in overcoming the action of drug resistance.

摘要

尽管维生素C在临床试验中无效,且抗氧化剂对癌症有矛盾的影响,但它已被用于癌症的补充和替代医学中。维生素C被发现可诱导对癌症的细胞毒性。然而,其作用机制尚未完全阐明,且维生素C对人类恶性黑色素瘤的影响尚未得到研究。本研究表明,毫摩尔浓度的维生素C可显著降低人类恶性黑色素瘤细胞的活力和侵袭性,并诱导其凋亡。与SK-MEL-28相比,维生素C对维莫非尼耐药细胞系A2058显示出更强的细胞毒性。相反,微摩尔浓度的维生素C促进细胞生长、迁移和细胞周期进程,并保护细胞免受线粒体应激。维莫非尼反常地激活了维莫非尼耐药的A2058中的RAS-RAF-MEK-ERK信号通路,然而,维生素C消除了这种激活。维生素C与维莫非尼对维莫非尼耐药的A2058显示出协同细胞毒性。体内试验表明,口服较低剂量(相当于0.5 g/70 kg)的维生素C会增加黑色素瘤的生长。因此,维生素C可能根据浓度发挥促黑色素瘤或抗黑色素瘤作用。高剂量维生素C与维莫非尼联合使用有望克服耐药作用。

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