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鞣花酸通过表皮生长因子受体(EGFR)途径抑制黑色素瘤细胞的增殖、迁移和侵袭。

Ellagic acid inhibits cell proliferation, migration, and invasion in melanoma via EGFR pathway.

作者信息

Wang Fan, Chen Jiangyan, Xiang Debing, Lian Xiaojuan, Wu Chunrong, Quan Jin

机构信息

Department of Oncology, Jiangjin District Central Hospital Chongqing 402260, China.

出版信息

Am J Transl Res. 2020 May 15;12(5):2295-2304. eCollection 2020.

PMID:32509220
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7270036/
Abstract

Ellagic acid (EA), a polyphenolic compound from pomegranate fruit extracts, has been reported to possess anti-proliferation, pro-apoptosis, and anti-invasion effects on many cancers. However, its effect on melanoma is yet to be clarified. In the present study, we investigated the anti-cancer effects of EA on melanoma cells and . The results indicated that 40 µM of EA significantly inhibited the proliferation, migration, and invasion of WM115 and A375 cells. The EA treatment significantly decreased the expression of p-EGFR and Vimentin, but increased the expression of E-cadherin in both cell lines. We further found that EGFR activation significantly abolished the effect of EA on WM115 and A375 cells. Moreover, EA treatment impaired tumorigenesis of A375 cells. Moreover, elevated pEGFR expression was an independent detrimental factor for melanoma patients. Taken together, our study provided evidence that EA treatment inhibits the migration, invasion and proliferation of melanoma cells via EGFR signaling pathway. These findings strongly suggested that EA might be useful for the development of new therapeutic strategies at melanoma.

摘要

鞣花酸(EA)是一种来自石榴果实提取物的多酚类化合物,据报道对多种癌症具有抗增殖、促凋亡和抗侵袭作用。然而,其对黑色素瘤的作用尚待阐明。在本研究中,我们研究了EA对黑色素瘤细胞的抗癌作用。结果表明,40 µM的EA显著抑制了WM115和A375细胞的增殖、迁移和侵袭。EA处理显著降低了p-EGFR和波形蛋白的表达,但增加了两种细胞系中E-钙黏蛋白的表达。我们进一步发现,EGFR激活显著消除了EA对WM115和A375细胞的作用。此外,EA处理损害了A375细胞的肿瘤发生。此外,pEGFR表达升高是黑色素瘤患者的一个独立有害因素。综上所述,我们的研究提供了证据表明EA处理通过EGFR信号通路抑制黑色素瘤细胞的迁移、侵袭和增殖。这些发现强烈表明EA可能有助于开发针对黑色素瘤的新治疗策略。

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Expression level of EGFR and MET receptors regulates invasiveness of melanoma cells.表皮生长因子受体和间质上皮转化因子受体的表达水平调节黑色素瘤细胞的侵袭性。
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