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铁皮石斛通过诱导细胞周期阻滞于G2/M期并调节关键生物标志物来抑制MCF-7细胞增殖。

Dendrobium candidum inhibits MCF-7 cells proliferation by inducing cell cycle arrest at G2/M phase and regulating key biomarkers.

作者信息

Sun Jing, Guo Yidi, Fu Xueqi, Wang Yongsen, Liu Ye, Huo Bo, Sheng Jun, Hu Xin

机构信息

School of Life Sciences, Jilin University, Changchun, People's Republic of China.

School of Life Sciences, Jilin University, Changchun, People's Republic of China; Key Laboratory for Molecular Enzymology and Engineering of Ministry of Education, Jilin University, Changchun, People's Republic of China; National Engineering Laboratory of AIDS Vaccine, School of Life Sciences, Jilin University, Changchun, People's Republic of China.

出版信息

Onco Targets Ther. 2015 Dec 21;9:21-30. doi: 10.2147/OTT.S93305. eCollection 2016.

DOI:10.2147/OTT.S93305
PMID:26730200
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4694679/
Abstract

BACKGROUND

Breast cancer is one of the most frequently occurring cancers in women. In recent years, Dendrobium candidum has played a part in antihyperthyroidism and anticancer drugs. This study aims to examine the antitumor effect of D. candidum on breast cancer.

METHODS

Human breast cancer cell line MCF-7 and normal breast epithelial cell line MCF10A were used to observe the effects of D. candidum treatment on human breast cancer. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was employed to examine the cell proliferation of the MCF-7 and MCF10A cells. Western blot analysis and reverse transcription polymerase chain reaction were used to detect the key molecules and biomarkers in breast cancer pathology. Cell cycle was analyzed by using Becton Dickinson FACScan cytofluorometer.

RESULTS

The results indicated that D. candidum significantly decreased cell viability at different concentrations compared to the control group (P<0.05). D. candidum-treated MCF-7 cells in the G2/M phase was significantly increased compared to the control group (P<0.05). The messenger RNA levels of estrogen receptor alpha, IGFBP2, IGFBP4, and GATA3 were significantly decreased, and the messenger RNA and protein levels of ELF5, p53, p21, p18, CDH1, CDH2, and p12 were significantly increased, compared to the control group (P<0.05). The protein levels of estrogen receptor alpha, PGR, GATA3, and Ki67 were significantly decreased and the protein levels of p53 and ELF5 were significantly increased compared to the control group (P<0.05). The general apoptosis biomarker, Bcl-2, was significantly decreased and the Bax was significantly increased compared to the control group (P<0.05). In contrast to that in MCF-7, D. candidum does not affect cell proliferation at any concentration and any time points in normal breast epithelial cells, MCF10A cells.

CONCLUSION

D. candidum could decrease the cell viability of MCF-7 cells by inducing cell cycle arrest at the G2/M phase and regulating the key biomarkers in breast cancer cells.

摘要

背景

乳腺癌是女性中最常见的癌症之一。近年来,铁皮石斛在抗甲状腺功能亢进和抗癌药物中发挥了作用。本研究旨在探讨铁皮石斛对乳腺癌的抗肿瘤作用。

方法

使用人乳腺癌细胞系MCF-7和正常乳腺上皮细胞系MCF10A来观察铁皮石斛处理对人乳腺癌的影响。采用3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四氮唑溴盐(MTT)法检测MCF-7和MCF10A细胞的增殖情况。使用蛋白质免疫印迹分析和逆转录聚合酶链反应检测乳腺癌病理学中的关键分子和生物标志物。使用贝克曼库尔特流式细胞仪分析细胞周期。

结果

结果表明,与对照组相比,不同浓度的铁皮石斛均显著降低细胞活力(P<0.05)。与对照组相比,经铁皮石斛处理的MCF-7细胞在G2/M期显著增加(P<0.05)。与对照组相比,雌激素受体α、胰岛素样生长因子结合蛋白2、胰岛素样生长因子结合蛋白4和GATA3的信使核糖核酸水平显著降低,而ELF5、p53、p21、p18、钙黏蛋白1、钙黏蛋白2和p12的信使核糖核酸和蛋白质水平显著升高(P<0.05)。与对照组相比,雌激素受体α、孕激素受体、GATA3和Ki67的蛋白质水平显著降低,而p53和ELF5蛋白质水平显著升高(P<0.05)。与对照组相比,一般凋亡生物标志物Bcl-2显著降低,而Bax显著升高(P<0.05)。与MCF-7细胞不同,铁皮石斛在任何浓度和任何时间点均不影响正常乳腺上皮细胞MCF10A细胞的增殖。

结论

铁皮石斛可通过诱导细胞周期阻滞在G2/M期并调节乳腺癌细胞中的关键生物标志物来降低MCF-7细胞的活力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0006/4694679/1aba248b3d28/ott-9-021Fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0006/4694679/c5de68a03158/ott-9-021Fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0006/4694679/ef16e658c85c/ott-9-021Fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0006/4694679/2e166de38427/ott-9-021Fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0006/4694679/1aba248b3d28/ott-9-021Fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0006/4694679/c5de68a03158/ott-9-021Fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0006/4694679/ef16e658c85c/ott-9-021Fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0006/4694679/2e166de38427/ott-9-021Fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0006/4694679/1aba248b3d28/ott-9-021Fig4.jpg

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