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没食子酸降低人宫颈癌细胞的细胞活力、增殖、侵袭和血管生成。

Gallic acid reduces cell viability, proliferation, invasion and angiogenesis in human cervical cancer cells.

作者信息

Zhao Bing, Hu Mengcai

机构信息

Department of Health, The Third Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450052, P.R. China.

出版信息

Oncol Lett. 2013 Dec;6(6):1749-1755. doi: 10.3892/ol.2013.1632. Epub 2013 Oct 15.

DOI:10.3892/ol.2013.1632
PMID:24843386
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4023842/
Abstract

Gallic acid is a trihydroxybenzoic acid, also known as 3,4,5-trihydroxybenzoic acid, which is present in plants worldwide, including Chinese medicinal herbs. Gallic acid has been shown to have cytotoxic effects in certain cancer cells, without damaging normal cells. The objective of the present study was to determine whether gallic acid is able to inhibit human cervical cancer cell viability, proliferation and invasion and suppress cervical cancer cell-mediated angiogenesis. Treatment of HeLa and HTB-35 human cancer cells with gallic acid decreased cell viability in a dose-dependent manner. BrdU proliferation and tube formation assays indicated that gallic acid significantly decreased human cervical cancer cell proliferation and tube formation in human umbilical vein endothelial cells, respectively. Additionally, gallic acid decreased HeLa and HTB-35 cell invasion . Western blot analysis demonstrated that the expression of ADAM17, EGFR, p-Akt and p-Erk was suppressed by gallic acid in the HeLa and HTB-35 cell lines. These data indicate that the suppression of ADAM17 and the downregulation of the EGFR, Akt/p-Akt and Erk/p-Erk signaling pathways may contribute to the suppression of cancer progression by Gallic acid. Gallic acid may be a valuable candidate for the treatment of cervical cancer.

摘要

没食子酸是一种三羟基苯甲酸,也被称为3,4,5 - 三羟基苯甲酸,它存在于世界各地的植物中,包括中草药。已表明没食子酸对某些癌细胞具有细胞毒性作用,而不会损害正常细胞。本研究的目的是确定没食子酸是否能够抑制人宫颈癌细胞的活力、增殖和侵袭,并抑制宫颈癌细胞介导的血管生成。用没食子酸处理HeLa和HTB - 35人癌细胞,细胞活力呈剂量依赖性降低。BrdU增殖和管形成试验表明,没食子酸分别显著降低人宫颈癌细胞的增殖和人脐静脉内皮细胞中的管形成。此外,没食子酸降低了HeLa和HTB - 35细胞的侵袭。蛋白质印迹分析表明,在HeLa和HTB - 35细胞系中,没食子酸抑制了ADAM17、表皮生长因子受体(EGFR)、磷酸化蛋白激酶B(p - Akt)和磷酸化细胞外信号调节激酶(p - Erk)的表达。这些数据表明,ADAM17的抑制以及EGFR、Akt/p - Akt和Erk/p - Erk信号通路的下调可能有助于没食子酸对癌症进展的抑制作用。没食子酸可能是治疗宫颈癌的一个有价值的候选药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b8bc/4023842/ea93c9a2c3e8/OL-06-06-1749-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b8bc/4023842/b249169ee164/OL-06-06-1749-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b8bc/4023842/a7d4e73d058a/OL-06-06-1749-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b8bc/4023842/656f1327ffbe/OL-06-06-1749-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b8bc/4023842/ea93c9a2c3e8/OL-06-06-1749-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b8bc/4023842/b249169ee164/OL-06-06-1749-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b8bc/4023842/a7d4e73d058a/OL-06-06-1749-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b8bc/4023842/656f1327ffbe/OL-06-06-1749-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b8bc/4023842/ea93c9a2c3e8/OL-06-06-1749-g03.jpg

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