这种20多元一盒的感冒药,竟有望“饿死”癌细胞
2017/11/25
“N-乙酰半胱氨酸(NAC)”是一种常用于缓解感冒症状的廉价药物,在一项最新的研究中,它被发现有着巨大的潜能:可以治疗癌症,通过“饿死”癌细胞阻止其生长、扩散。


11月10日,《Seminars in Oncology》期刊在线发表了一篇文章,揭示了这一“老药新用”的新成果

NAC

NAC是一种非处方药和膳食补充剂,通常用于缓解感冒、流感症状,例如咳嗽、喘息和流鼻涕等。此外,NAC也可以适用于乙酰氨基酚过量、囊性纤维化和慢性阻塞性肺病。作为一种普通药物,它的价格也相对廉价,一盒10s装的NAC片售价在20多元。

NAC具有抗氧化性,这意味着它能够减少由氧化应激引发的细胞损伤。之前已有研究表明,肿瘤基质细胞的氧化应激水平很高,特别是乳腺癌肿瘤。当肿瘤的基质细胞暴露于氧化应激中,它们会释放出乳酸及其他“营养物质”,促进肿瘤的生长。

考虑到这两点,文章作者、索尔福德大学Federica Sotgia和团队推测,NAC的抗氧化特性或许可以“饿死”癌细胞。

令人鼓舞的结果

为了验证猜想,研究团队招募了12名0期或者1期乳腺癌女性患者,进行相关试验。在患者从确诊到接受手术治疗之间的3周内,她们会接受NAC治疗,包括每周一次的静脉注射(每次剂量为150mg/公斤),以及每日(静脉注射那日除外)服用两次NAC药片(每次剂量为600mg)。

在手术前和手术后,患者的肿瘤组织都会接受活检分析,重点关注3个标志物(与癌症恶化、总体生存期差有关):MCT4、CAV1和Ki67。结果显示,Ki67的水平降低了25%,而MCT4的水平则降低了80%。

这意味着,NAC能够以无毒的方式抑制MCT4蛋白的表达,从而阻止癌细胞的生长、分裂。

Sotgia团队希望,这一最新研究能够“重新附能”FDA已经批准的廉价药物,从而给癌症治疗带来新的选择。

参考资料:

Cancer cell growth halted with cold and flu drug

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  • Pilot study demonstrating metabolic and anti-proliferative effects of in vivo anti-oxidant supplementation with N-Acetylcysteine in Breast Cancer

    Background High oxidative stress as defined by hydroxyl and peroxyl activity is often found in the stroma of human breast cancers. Oxidative stress induces stromal catabolism, which promotes cancer aggressiveness. Stromal cells exposed to oxidative stress release catabolites such as lactate, which are up-taken by cancer cells to support mitochondrial oxidative phosphorylation. The transfer of catabolites between stromal and cancer cells leads to metabolic heterogeneity between these cells and increased cancer cell proliferation and reduced apoptosis in preclinical models. N-Acetylcysteine (NAC) is an antioxidant that reduces oxidative stress and reverses stromal catabolism and stromal-carcinoma cell metabolic heterogeneity, resulting in reduced proliferation and increased apoptosis of cancer cells in experimental models of breast cancer. The purpose of this clinical trial was to determine if NAC could reduce markers of stromal-cancer metabolic heterogeneity and markers of cancer cell aggressiveness in human breast cancer. Methods Subjects with newly diagnosed stage 0 and I breast cancer who were not going to receive neoadjuvant therapy prior to surgical resection were treated with NAC before definitive surgery to assess intra-tumoral metabolic markers. NAC was administered once a week intravenously at a dose of 150 mg/kg and 600 mg twice daily orally on the days not receiving intravenous NAC. Histochemistry for the stromal metabolic markers monocarboxylate transporter 4 (MCT4) and caveolin-1 (CAV1) and the Ki67 proliferation assay and TUNEL apoptosis assay in carcinoma cells were performed in pre- and post-NAC specimens. Results The range of days on NAC was 14–27 and the mean was 19 days. Post-treatment biopsies showed significant decrease in stromal MCT4 and reduced Ki67 in carcinoma cells. NAC did not significantly change stromal CAV1 and carcinoma TUNEL staining. NAC was well tolerated. Conclusions NAC as a single agent reduces MCT4 stromal expression, which is a marker of glycolysis in breast cancer with reduced carcinoma cell proliferation. This study suggests that modulating metabolism in the tumor microenvironment has the potential to impact breast cancer proliferation.

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