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L.花提取物抑制人结肠癌细胞系和肺癌细胞系的细胞生长及转移特性。

L. flower extract inhibits cell growth and metastatic properties in human colon and lung cancer cell lines.

作者信息

Seo Jina, Lee Jungjae, Yang Hyi Young, Ju Jihyeung

机构信息

Department of Food and Nutrition Chungbuk National University Cheongju Korea.

出版信息

Food Sci Nutr. 2020 Oct 1;8(11):6259-6268. doi: 10.1002/fsn3.1924. eCollection 2020 Nov.

DOI:10.1002/fsn3.1924
PMID:33282275
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7684585/
Abstract

Snapdragon L.) flowers are one of the most frequently used edible flowers in different preparations of foods and drinks. In this study, we examined inhibitory effects of snapdragon flower extract (SFE) against distinctive properties of cancer cells, stimulated growth, and activated metastasis, using H1299 lung cancer and HCT116 colon cancer cell lines. SFE treatment at 100-1,000 μg/ml for 24-72 hr resulted in a time- and dose-dependent growth inhibition in H1299 and HCT116 cells. Cell cycle analysis and Annexin V staining assay further revealed that SFE caused cell cycle arrest at G2/M phase and induction of apoptosis, indicating the growth inhibition by SFE is attributed to its G2/M cell cycle-arresting and apoptosis-inducing activities. SFE dose-dependently enhanced generation of intracellular reactive oxygen species (ROS) and reduced mitochondrial membrane potential in H1299 cells but had no effect on intracellular ROS levels in HCT116 cells, suggesting that the type of apoptosis induced by SFE in H1299 cells is different to that in HCT116 cells. Furthermore, SFE alleviated invasion, levels of matrix metalloproteinases, migration, and adhesion in H1299 and HCT116 cells. These results indicate that SFE not only inhibits cell growth by cell cycle arrest at G2/M and apoptosis induction but also alleviates metastatic properties such as invasion, migration, and adhesion in lung and colon cancer cells.

摘要

金鱼草(Antirrhinum majus L.)花是食品和饮料不同制剂中最常用的可食用花卉之一。在本研究中,我们使用H1299肺癌细胞系和HCT116结肠癌细胞系,研究了金鱼草花提取物(SFE)对癌细胞独特特性、刺激生长和激活转移的抑制作用。在100 - 1000μg/ml浓度下处理24 - 72小时,SFE对H1299和HCT116细胞的生长抑制呈时间和剂量依赖性。细胞周期分析和膜联蛋白V染色试验进一步表明,SFE导致细胞周期停滞在G2/M期并诱导细胞凋亡,这表明SFE的生长抑制作用归因于其G2/M期细胞周期阻滞和凋亡诱导活性。SFE剂量依赖性地增强了H1299细胞内活性氧(ROS)的产生并降低了线粒体膜电位,但对HCT116细胞内ROS水平没有影响,这表明SFE在H1299细胞中诱导的凋亡类型与在HCT116细胞中不同。此外,SFE减轻了H1299和HCT116细胞的侵袭、基质金属蛋白酶水平、迁移和粘附。这些结果表明,SFE不仅通过使细胞周期停滞在G2/M期和诱导凋亡来抑制细胞生长,还减轻了肺癌和结肠癌细胞的转移特性,如侵袭、迁移和粘附。

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