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Differentially Expressed Apoptosis-Related Genes Profile of T47D Breast Cancer Cells Treated With Angiotensin-(1-7)

机译:用血管紧张素 - (1-7)处理的T47D乳腺癌细胞的差异表达凋亡相关基因谱

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Angiotensin-(1-7) [Ang-(1-7)] is an endogenous seven-aminoacid peptide hormone of the reninangiotensinsystem that has antiproliferative properties. Recent studies suggest that Ang-(1-7) inhibits growth oflung cancer cells through reduction in cellular proliferation and induction of apoptosis. The aim of this work is toassess the pro-apoptotic effects of Ang-(1-7) in breast cancer cells (T47D). Methods: T47D cells were treatedwith angiotensin-(1-7) (10-6M) for 48 hours. The percentage of apoptotic cells was measured by flow cytometry(Millipore guava). In addition, we used the SA Biosciences Human Apoptosis RT2 Profiler PCR Array profiles toanalyze the expression of 84 key genes involved in programmed cell death. Network analyses of differentiallyexpressed genes were performed through MetaCore database (GeneGo). Ang-(1-7) caused a significantly higherrate of apoptosis than the control group. More than 60% of the apoptosis-related-genes were differentiallyexpressed, of which approximately 50% genes were up-regulated, such as TNF, BCL2, BAX and BIK, whichhave shown to be nineteen fifteen, nine and four times more expressed, respectively, than control. Furthermore,seventeen regulatory gene networks were derived from MetaCore analysis, suggesting the molecularmechanisms underlying of apoptotic-driven T47D cells. Conclusions: In summary, it is clear that Ang-(1-7)induces apoptosis in T47D breast cancer cells and it probably does so through activation of BCL2 gene familyand TNF related genes.
机译:血管紧张素 - (1-7)[Ang-(1-7)]是具有抗增殖性质的雷纳天皂虫系统的内源性七氨基酸肽激素。最近的研究表明,Ang-(1-7)通过降低细胞增殖和诱导细胞凋亡来抑制肺癌细胞的生长。这项工作的目的是拍摄乳腺癌细胞(T47D)中Ang-(1-7)的促凋亡作用。方法:将T47D细胞处理过血管紧张素 - (1-7)(10-6米)48小时。通过流式细胞术(Millipore Guava)测量凋亡细胞的百分比。此外,我们使用SA Biosciences人细胞凋亡RT2分析PCR阵列曲线来分析84个关键基因的表达参与编程的细胞死亡。通过Metacore Database(Genego)进行差异化基因的网络分析。 Ang-(1-7)引起了比对照组的显着升高。超过60%的细胞凋亡相关基因差异化,其中约50%基因被上调,例如TNF,BCL2,BAX和BIK,其显示为九十五,九个和四倍,分别更新而不是控制。此外,源自凋亡驱动的T47D细胞的分子机制,源自凋亡驱动的T47D细胞的分子机制。结论:总之,显然Ang-(1-7)诱导T47D乳腺癌细胞中的细胞凋亡,并且通过激活Bcl2基因家庭和TNF相关基因可能会产生这种情况。

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