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阿霉素诱导小鼠MCF-7乳腺癌细胞凋亡和抑制增殖的体内实验研究 被引量:1

In vivo study on apoptosis and cell proliferation induced by adriamycin in mice with MCF-7 breast cancer
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摘要 目的:探讨阿霉素对荷瘤鼠MCF7乳腺癌细胞凋亡和增殖的影响。方法:建立小鼠MCF7乳腺癌细胞模型,用TUNEL法和免疫组化法检测阿霉素作用下MCF7乳腺癌细胞的凋亡和PCNA表达的变化。结果:1.25mg·kg-1阿霉素的抑瘤率为43%。MCF7乳腺癌细胞的凋亡指数为1.93%,较荷瘤对照组的1.11%明显升高(P<0.05)。增殖指数为35.75%,较荷瘤对照组的56.38%明显下降(P<0.01)。结论:阿霉素有诱导小鼠MCF7乳腺癌细胞凋亡和抑制其增殖的作用。 AIM: To observe the apoptosis and cell proliferation induced by adriamycin in mice with breast cancer. METHODS: Therapeutic effect of 1.25 mg·kg -1 adriamycin (ADR) on mice MCF-7 breast cancer was observed in vivo. Apoptosis and PCNA of tumor cells were also studied by TUNEL and immunohistochemical methods. RESULTS: In the control group, the apoptotic cell index (AI) in tumor cell was 1.11% and PCNA index (PI) was 56.38%. In the ADR group, the rate of tumor inhibition was 43% and the AI was 1.93% (P< 0.05). The 35.75% of PI in ADR group was lower than that in the control group (P< 0.01). CONCLUSION: Adriamycin may induce apoptosis and reduce cell proliferation.
出处 《中国临床药理学与治疗学》 CAS CSCD 2005年第6期674-676,共3页 Chinese Journal of Clinical Pharmacology and Therapeutics
基金 湖南省卫生厅课题基金项目(№2001Y58)
关键词 阿霉素 乳腺肿瘤 细胞凋亡 增殖细胞核抗原 adriamycin breast neoplasm apoptosis PCNA
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参考文献7

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同被引文献6

  • 1郑建勇,李开宗,王为忠,管文贤,易军.阿霉素诱导人肝癌细胞凋亡机制的研究[J].中国普通外科杂志,2005,14(7):509-511. 被引量:6
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  • 3Bell DR,Van Zant G.Stem cells,aging,and cancer:inevitabilities and outcomes[J].Oncogene,2004,23(43):7290-7296.
  • 4Li QQ,Xu JD,Wang WJ,et al.Twist1-mediated adriamycin-induced epithelial-mesenchymal transition relates to multidrug resistance and invasive potential in breast cancer cells[J].Clin Cancer Res,2009,15(8):2657-2665.
  • 5Dontu G,Abdallah WM,Foley JM,et al.In vitro propagation and transcriptional profiling of human mammary stem/progenitor cells[J].Genes Dev,2003,17(10):1253-1270.
  • 6Serrano D,Bleau AM,Fernandez-Garcia I,et al.Inhibition of telomerase activity preferentially targets aldehyde dehydrogenasepositive cancer stem-like cells in lung cancer[J].Mol Cancer,2011,10(1):96.

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