| 芹菜素诱导乳腺癌T47D细胞系p53依赖性凋亡及G2/M期阻滞 |
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| 引用本文： | 刘博文,张斌,张月,冯炜红,李媛媛,张伟然,曹旭晨. 芹菜素诱导乳腺癌T47D细胞系p53依赖性凋亡及G2/M期阻滞[J]. 中国肿瘤临床, 2012, 39(6): 315-317. DOI: 10.3969/j.issn.1000-8179.2012.02.006.004 |
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| 作者姓名： | 刘博文 张斌 张月 冯炜红 李媛媛 张伟然 曹旭晨 |
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| 作者单位： | 天津医科大学附属肿瘤医院乳腺一科，教育部乳腺癌防治重点实验室，天津市肿瘤防治重点实验室（天津市 300060） |
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| 基金项目： | 本文课题受国家自然科学基金,天津市应用基础及前沿技术研究计划基金 |
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| 摘 要： | 目的 探讨芹菜素（apigenin）对乳腺癌T47D细胞系凋亡及细胞周期的影响。 方法 常规培养T47D细胞, 用四甲基偶氮唑盐法（MTT法）检测芹菜素对乳腺癌T47D细胞系细胞增殖的影响。荧光染色法观察凋亡细胞的形态变化。流式细胞仪检测细胞凋亡率及周期分布。Western blot检测不同浓度（0、10、20、40、80 μM）芹菜素对凋亡及周期相关蛋白表达的影响。 结果 随着芹菜素浓度的增加, 芹菜素对T47D细胞的增殖抑制作用明显增强（P < 0.05）; 凋亡荧光染色及流式细胞仪显示, 芹菜素能够诱导乳腺癌T47D细胞凋亡, 随着其浓度的增高, 各组凋亡率分别为（2.41±0.072）%、（10.87±0.028）%、（18.02±0.056）%、（37.05± 0.092）%和（78.38±0.082）%, 与对照组相比, 差异有统计学意义（P < 0.05）; 流式周期分析显示, 芹菜素能够使T47D细胞系G2/M期阻滞, 随着芹菜素浓度的增高, 不同浓度组细胞G2/M期所占的比例逐渐增加, 差异有统计学意义（P < 0.05）; Western blot显示p53、p21、Bax和p-Cdc2的含量及Caspase-3, PARP剪切明显增加, 而Bcl-2、CyclinB1及Cdc2的含量却显著减少。 结论 芹菜素能够诱导乳腺癌T47D细胞系p53依赖性凋亡及G2/M期阻滞, 从而明显抑制其增殖。
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| 关 键 词： | 芹菜素 乳腺癌细胞 凋亡 细胞周期 |
| 收稿时间： | 2011-06-20 |
Apigenin Induces p53-Dependent Apoptosis and G2/M Arrest in Breast Cancer T47D Cells |
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| Bowen LIU , Bin ZHANG , Yue ZHANG , Weihong FENG , Yuanyuan LI , Weiran ZHANG , Xuchen CAO. Apigenin Induces p53-Dependent Apoptosis and G2/M Arrest in Breast Cancer T47D Cells[J]. Chinese Journal of Clinical Oncology, 2012, 39(6): 315-317. DOI: 10.3969/j.issn.1000-8179.2012.02.006.004 |
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| Authors: | Bowen LIU Bin ZHANG Yue ZHANG Weihong FENG Yuanyuan LI Weiran ZHANG Xuchen CAO |
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| Affiliation: | The First Department of Breast Oncology, Tianjin Medical University Cancer Institute and Hospital, Key Laboratory of Breast CancerPrevention and Treatment of the Ministry of Education, Key Laboratory of Cancer Prevention and Treatment of Tianjin City, Tianjin 300060, China |
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| Abstract: | Objective The present study aims to investigate the effects of apigenin on the proliferation breast cancer of T47D cell line. Methods T47D cells were cultured in vitro. Cell proliferation was measured by MTT assay. Morphological changes in the apoptotic cells were observed by a fluorescent microscope. Flow cytometry was used to detect the ratio of apoptotic cells and cell cycle distribution. Western blot analysis was used to detect the apoptosis- and cycle-related protein. Results MTT showed that apigenin could inhibit the proliferation of T47D cells in a dose-dependent manner (P < 0.05). Fluorescent staining and flow cytometry showed a significant increase in the apoptosis of T47D cells after apigenin treatment, and the apoptotic ratios of the different groups were (2.41 ± 0.072)%, (10.87 ±0.028) %, (18.02 ±0.056) %, (37.05 ±0.092) %, and (78.38 ±0.082) %, respectively, with a statistically significant difference (P < 0.05). Apigenin could induce G2/M arrest of T47D cells, and the ratio of G2/M phase increased with increasing concentration of apigenin (P < 0.05). The cleaved PARP, caspase3, p53, p21, Bax, and p-Cdc2 significantly increased, whereas Bcl-2, cyclin B1, and Cdc2 expression decreased. Conclusion Apigenin could induce p53-dependent apoptosis and G2/M arrest of the breast cancer T47D cell line. |
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