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大黄素通过调节凋亡相关基因的表达诱导人乳腺癌细胞凋亡。

Emodin induces apoptosis of human breast cancer cells by modulating the expression of apoptosis-related genes.

作者信息

Zu Cong, Zhang Mingdi, Xue Hui, Cai Xiaopeng, Zhao Lei, He Anning, Qin Guangyuan, Yang Chunshu, Zheng Xinyu

机构信息

Lab 1, Cancer Institute, China Medical University, Shenyang, Liaoning 110001, P.R. China.

Department of General Surgery, Xinhua Hospital, Shanghai Jiaotong University, School of Medicine, Shanghai 200092, P.R. China.

出版信息

Oncol Lett. 2015 Nov;10(5):2919-2924. doi: 10.3892/ol.2015.3646. Epub 2015 Aug 26.

DOI:10.3892/ol.2015.3646
PMID:26722264
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4665964/
Abstract

The aim of this study was to investigate the effects of emodin on the proliferation of human breast cancer cells Bcap-37 and ZR-75-30. Cell viability following emodin treatment was assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The effects of emodin on apoptosis were determined by flow cytometry using Annexin V-fluorescein isothiocyanate and propidium iodide staining. Quantitative polymerase chain reaction and western blot analysis were used to determine changes in the expression of apoptotic genes and protein, respectively. The effect of emodin on the invasiveness of breast cancer cells was evaluated by Matrigel invasion assay. Treatment of breast cancer cells Bcap-37 and ZR-75-30 with emodin was observed to inhibit the growth and induced apoptosis in a time- and dose-dependent manner. Emodin reduced the level of Bcl-2 and increased levels of cleaved caspase-3, PARP, p53 and Bax. These findings indicate that emodin induces growth inhibition and apoptosis in human breast cancer cells. Emodin may be a potential therapeutic agent for the treatment of breast cancer.

摘要

本研究旨在探讨大黄素对人乳腺癌细胞Bcap - 37和ZR - 75 - 30增殖的影响。采用3-(4,5 - 二甲基噻唑 - 2 - 基)-2,5 - 二苯基四氮唑溴盐(MTT)法评估大黄素处理后的细胞活力。使用膜联蛋白V - 异硫氰酸荧光素和碘化丙啶染色,通过流式细胞术测定大黄素对细胞凋亡的影响。分别采用定量聚合酶链反应和蛋白质印迹分析来确定凋亡基因和蛋白表达的变化。通过基质胶侵袭试验评估大黄素对乳腺癌细胞侵袭性的影响。观察到用大黄素处理乳腺癌细胞Bcap - 37和ZR - 75 - 30可抑制其生长并诱导凋亡,且呈时间和剂量依赖性。大黄素降低了Bcl - 2的水平,增加了裂解的半胱天冬酶 - 3、聚(ADP - 核糖)聚合酶、p53和Bax的水平。这些发现表明大黄素可诱导人乳腺癌细胞生长抑制和凋亡。大黄素可能是一种治疗乳腺癌的潜在治疗药物。

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本文引用的文献

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Emodin suppresses Wnt signaling in human colorectal cancer cells SW480 and SW620.大黄素抑制人结肠癌细胞SW480和SW620中的Wnt信号通路。
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Emodin inhibits breast cancer cell proliferation through the ERα-MAPK/Akt-cyclin D1/Bcl-2 signaling pathway.大黄素通过雌激素受体α-丝裂原活化蛋白激酶/蛋白激酶B-细胞周期蛋白D1/凋亡蛋白Bcl-2信号通路抑制乳腺癌细胞增殖。
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