Mucoxin (Acetogenin) Inhibits Proliferation of T47D Breast Cancer by Suppressing Expression of Cyclin D1 Mediated by p53

Muhartono Muhartono, Sutyarso Sutyarso, M. Kanedi
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引用次数: 2

Abstract

Background: Mucoxinis believed to be a promising anticancer because it is known to inhibit cell proliferation. However, given study on mucoxin still very limited, the mechanism of the substances isolated from leaf extract of Rollinia mucosa in regulating and eliminating cancer cells has not fully understood. This study investigated the mucoxin mechanism in affecting proliferation, expression of p53 and cyclin D1 genes in the T47D breast cancer cells. Materials and Methods: The cell line samples were grouped into four referred to the hour of assays undertaken after mucoxin application, namely hour 0th, 24th, 48th and 72nd. Each group was given mucoxin of six different concentrations namely 0.00 µg mLG 1 as a control, 0.1×10G 3 , 0.5×10G 3 , 1×10G 3 , 5×10G 3 and 10×10 S3 µg mLG with three replications. Cells proliferation assayed by flow cytometry technique using BrDU staining protocol, whereas the expression of p53 and cyclin D1 genes determined by quantitative PCR (qPCR). Results: Cell proliferation in each group significantly reduced by mucoxin treatment. and 10×10 Mucoxin enhance p53 gene expression in 48 h, while the expression of cyclin D1 supressed signifantly by mucoxin of 5×10G S3 µ g mL G in 48 and 72 h. Simple regression analysis showed that cell proliferation decreased with the increase of p53 expression and the suppression of cyclin D1 gene, while p53 expression positively associated to cyclin D1 expression. Conclusion: Mucoxin can 1 decrease the proliferation of T47D breast cancer cells by suppressing the expression of cyclin D1 mediated by p53 gene.
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Mucoxin (Acetogenin)通过抑制p53介导的Cyclin D1表达抑制T47D乳腺癌的增殖
背景:粘液毒素被认为是一种很有前途的抗癌药物,因为它可以抑制细胞增殖。然而,由于对黏液毒素的研究还很有限,从铃兰黏膜叶提取物中分离出的物质调节和消灭癌细胞的机制尚不完全清楚。本研究探讨粘毒素影响T47D乳腺癌细胞增殖及p53、cyclin D1基因表达的机制。材料与方法:将细胞系样品按黏液毒素应用后第0小时、第24小时、第48小时、第72小时的检测时间分为4组。每组分别给予6种不同浓度的黏液毒素,分别为0.00µg mLG 1作为对照,0.1×10G 3、0.5×10G 3、1×10G 3、5×10G 3和10×10 S3µg mLG,重复3次。流式细胞术采用BrDU染色检测细胞增殖,定量PCR检测p53和cyclin D1基因的表达。结果:黏液毒素处理后各组细胞增殖能力明显降低。和10×10粘毒素可在48 h内增强p53基因的表达,而5×10G S3µg mL g的粘毒素可在48和72 h内显著抑制cyclin D1的表达。简单回归分析显示,细胞增殖随着p53表达的增加和cyclin D1基因的抑制而降低,而p53的表达与cyclin D1的表达呈正相关。结论:黏液毒素可通过抑制p53基因介导的细胞周期蛋白D1的表达来抑制T47D乳腺癌细胞的增殖。
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