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异麦角甾苷对人卵巢癌体外和体内生长的抑制作用是通过亚G1期细胞周期停滞、活性氧生成以及AKT/PI3K/m-TOR信号通路的调节介导的。

Suppression of in vitro and in vivo human ovarian cancer growth by isoacteoside is mediated via sub-G1 cell cycle arrest, ROS generation, and modulation of AKT/PI3K/m-TOR signalling pathway.

作者信息

Yang Xili, Guo Fei, Peng Qingmei, Liu Yang, Yang Bin

机构信息

Department of Anesthesiology, Shanghai First Maternity and Infant Hospital, Tongji University School of Medicine, Shanghai 200120, China.

出版信息

J BUON. 2019 Jan-Feb;24(1):285-290.

PMID:30941982
Abstract

PURPOSE

The purpose of the present study was to investigate the anticancer properties of isoacteoside against OVCAR-3 human ovarian cancer cells. Its effects on apoptosis, reactive oxygen species (ROS) generation, cell invasion, cell cycle arrest and its effects on tumor volume and weight were also evaluated in the current study.

METHODS

MTT assay was used to study the cytotoxic effects of the compound on the cell viability. Effects on apoptosis and cell cycle arrest were evaluated by flow cytometry. In vitro wound healing assay and matrigel assay were carried out to study the effects of isoacteoside on cell migration and cell invasion respectively. Non-cancer ovarian cell line SV-40 served as control.

RESULTS

Isoacteoside exerted both dose-dependent as well as time-dependent growth inhibitory effects on ovarian cancer cells with IC50 values of 15 µM at 24h incubation. Isoacteoside led to early and late apoptosis induction in these cells. Isoacteoside also led to sub-G1 cell cycle arrest which showed strong dose-dependence. Isoacteoside treatment also led to inhibition of cell migration and cell invasion. The results revealed that OVCAR-3 tumor growth was significantly suppressed by isoacteoside administration, compared with that in the control group. At the end of the 5-week period of isoacteoside treatment, the average tumor growth and volume in the untreated control group were considerably higher than those in the treated groups.

CONCLUSION

In brief, the current study indicates that isoacteoside has a great potential in suppressing both in vitro and in vivo ovarian cancer cell growth and can be used as a possible anticancer agent.

摘要

目的

本研究旨在探究异秦皮苷对人卵巢癌细胞OVCAR-3的抗癌特性。本研究还评估了其对细胞凋亡、活性氧(ROS)生成、细胞侵袭、细胞周期阻滞的影响以及对肿瘤体积和重量的影响。

方法

采用MTT法研究该化合物对细胞活力的细胞毒性作用。通过流式细胞术评估对细胞凋亡和细胞周期阻滞的影响。分别进行体外伤口愈合试验和基质胶试验,以研究异秦皮苷对细胞迁移和细胞侵袭的影响。非癌性卵巢细胞系SV-40作为对照。

结果

异秦皮苷对卵巢癌细胞具有剂量依赖性和时间依赖性的生长抑制作用,在孵育24小时时IC50值为15μM。异秦皮苷导致这些细胞早期和晚期凋亡诱导。异秦皮苷还导致亚G1期细胞周期阻滞,表现出强烈的剂量依赖性。异秦皮苷处理还导致细胞迁移和细胞侵袭受到抑制。结果显示,与对照组相比,异秦皮苷给药显著抑制了OVCAR-3肿瘤生长。在异秦皮苷治疗5周结束时,未治疗的对照组的平均肿瘤生长和体积明显高于治疗组。

结论

简而言之,本研究表明异秦皮苷在抑制体外和体内卵巢癌细胞生长方面具有巨大潜力,可作为一种可能的抗癌药物。

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