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茶多酚通过抑制生存素的表达诱导乳腺癌细胞凋亡。

Tea polyphenols induced apoptosis of breast cancer cells by suppressing the expression of Survivin.

作者信息

Chen Xuesong, Li Yu, Lin Qiushi, Wang Yan, Sun Hong, Wang Jian, Cui Guoquan, Cai Li, Dong Xiaoqun

机构信息

1] Department of Internal Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang Province, China [2].

1] Bacteriologic Laboratory, Harbin Center for Disease Control and Prevention, Harbin, Heilongjiang Province, China [2].

出版信息

Sci Rep. 2014 Mar 20;4:4416. doi: 10.1038/srep04416.

DOI:10.1038/srep04416
PMID:24646833
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3960584/
Abstract

To study the mechanism of tea polyphenols (TP)-induced apoptosis of breast cancer cells. Proliferation of MCF-7 and SK-BR-3 cells was evaluated by MTT assays. Cellular ultrastructure was examined by electron microscopy. Apoptosis was detected by TUNEL. PCNA、 Cyclin D1、 Cyclin E and Survivin expression was measured by Western blot. Cell proliferation was significantly inhibited by TP. Spindle and round cells were loosely distributed with increased particles after TP treatment. Increased cell size, frequent nuclear atypia and a collapse of apoptosis were observed. The nucleus was pushed towards one side, while the cytoplasm was rich in free ribosome. The membrane of mitochondria was thickening, and the cell apoptotic body was observed. TP treated cells experienced significantly enhanced apoptosis compared with 5-Fu treated or control groups. The expression of survivin was downregulated by TP. To conclude, TP can inhibit cell growth and induce apoptosis through downregulating the expression of survivin in breast cancer.

摘要

研究茶多酚(TP)诱导乳腺癌细胞凋亡的机制。采用MTT法评估MCF-7和SK-BR-3细胞的增殖情况。通过电子显微镜检查细胞超微结构。采用TUNEL法检测细胞凋亡。通过蛋白质免疫印迹法检测PCNA、细胞周期蛋白D1、细胞周期蛋白E和生存素的表达。TP可显著抑制细胞增殖。TP处理后,纺锤形和圆形细胞分布松散,颗粒增多。观察到细胞体积增大、核异型频繁及凋亡增加。细胞核被挤向一侧,而细胞质富含游离核糖体。线粒体膜增厚,并观察到细胞凋亡小体。与5-氟尿嘧啶处理组或对照组相比,TP处理的细胞凋亡显著增强。TP可下调生存素的表达。总之,TP可通过下调乳腺癌中生存素的表达来抑制细胞生长并诱导细胞凋亡。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/94bf/3960584/e317a091ad48/srep04416-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/94bf/3960584/3b54b3a652ab/srep04416-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/94bf/3960584/9d67060dbc3f/srep04416-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/94bf/3960584/0518c7b0c1e8/srep04416-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/94bf/3960584/1cdcf11ea6de/srep04416-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/94bf/3960584/3a22146adc54/srep04416-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/94bf/3960584/e317a091ad48/srep04416-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/94bf/3960584/3b54b3a652ab/srep04416-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/94bf/3960584/9d67060dbc3f/srep04416-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/94bf/3960584/0518c7b0c1e8/srep04416-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/94bf/3960584/1cdcf11ea6de/srep04416-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/94bf/3960584/3a22146adc54/srep04416-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/94bf/3960584/e317a091ad48/srep04416-f6.jpg

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