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丹皮酚 C 通过巨胞饮作用和下调 Dickkopf 相关蛋白-3 抑制 YD-10B 人舌癌细胞的生长。

Meridianin C inhibits the growth of YD-10B human tongue cancer cells through macropinocytosis and the down-regulation of Dickkopf-related protein-3.

机构信息

Department of Molecular Medicine, College of Medicine, Keimyung University, Daegu, Republic of Korea.

Department of Chemistry, College of Natural Sciences, Keimyung University, Daegu, Republic of Korea.

出版信息

J Cell Mol Med. 2018 Dec;22(12):5833-5846. doi: 10.1111/jcmm.13854. Epub 2018 Sep 24.

Abstract

Meridianin C is a marine natural product known for its anti-cancer activity. At present, the anti-tumour effects of meridianin C on oral squamous cell carcinoma are unknown. Here, we investigated the effect of meridianin C on the proliferation of four different human tongue cancer cells, YD-8, YD-10B, YD-38 and HSC-3. Among the cells tested, meridianin C most strongly reduced the growth of YD-10B cells; the most aggressive and tumorigenic of the cell lines tested. Strikingly, meridianin C induced a significant accumulation of macropinosomes in the YD-10B cells; confirmed by the microscopic and TEM analysis as well as the entry of FITC-dextran, which was sensitive to the macropinocytosis inhibitor amiloride. SEM data also revealed abundant long and thin membrane extensions that resemble lamellipodia on the surface of YD-10B cells treated with meridianin C, pointing out that meridianin C-induced macropinosomes was the result of macropinocytosis. In addition, meridianin C reduced cellular levels of Dickkopf-related protein-3 (DKK-3), a known negative regulator of macropinocytosis. A role for DKK-3 in regulating macropinocytosis in the YD-10B cells was confirmed by siRNA knockdown of endogenous DKK-3, which led to a partial accumulation of vacuoles and a reduction in cell proliferation, and by exogenous DKK-3 overexpression, which resulted in a considerable inhibition of the meridianin C-induced vacuole formation and decrease in cell survival. In summary, this is the first study reporting meridianin C has novel anti-proliferative effects via macropinocytosis in the highly tumorigenic YD-10B cell line and the effects are mediated in part through down-regulation of DKK-3.

摘要

希替普兰 C 是一种海洋天然产物,以其抗癌活性而闻名。目前,希替普兰 C 对口腔鳞状细胞癌的抗肿瘤作用尚不清楚。在这里,我们研究了希替普兰 C 对四种不同的人舌癌细胞 YD-8、YD-10B、YD-38 和 HSC-3 的增殖的影响。在测试的细胞中,希替普兰 C 最强烈地减少了 YD-10B 细胞的生长;在测试的细胞系中最具侵袭性和致瘤性。引人注目的是,希替普兰 C 在 YD-10B 细胞中诱导了大量的巨胞饮泡的积累;通过显微镜和 TEM 分析以及 FITC-葡聚糖的进入证实,FITC-葡聚糖对巨胞饮抑制剂氨氯吡咪敏感。SEM 数据还显示,在希替普兰 C 处理的 YD-10B 细胞表面,存在大量的长而细的膜延伸,类似于片状伪足,表明希替普兰 C 诱导的巨胞饮泡是巨胞饮的结果。此外,希替普兰 C 降低了细胞内 Dickkopf 相关蛋白-3(DKK-3)的水平,DKK-3 是巨胞饮的已知负调节剂。通过内源性 DKK-3 的 siRNA 敲低证实了 DKK-3 在调节 YD-10B 细胞中的巨胞饮作用,导致空泡部分积累和细胞增殖减少,以及通过外源性 DKK-3 过表达,导致希替普兰 C 诱导的空泡形成显著抑制和细胞存活率降低。总之,这是第一项报道希替普兰 C 通过在高度致瘤性 YD-10B 细胞系中的巨胞饮作用具有新的抗增殖作用的研究,部分作用是通过下调 DKK-3 介导的。

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