本文選題：乳腺腫瘤 + 基因沉默�。� 參考：《腫瘤》2017年06期

【摘要】：目的:探討上皮細胞轉(zhuǎn)化序列2癌基因(epithelial cell transforming sequence 2 oncogene,ECT 2)沉默對乳腺癌細胞增殖和凋亡的影響,以及其潛在的作用機制。方法:首先采用實時熒光定量PCR和蛋白質(zhì)印跡法檢測正常乳腺上皮細胞(MCF-10A)和乳腺癌細胞(MDA-MB-231、SK-BR-3、MCF-7和BT474)中ECT2 mRNA及蛋白的表達水平。將特異性靶向沉默ECT 2基因的siRNA(ECT2 siRNA)轉(zhuǎn)染至乳腺癌MDA-MB-231和MCF-7細胞,并用細胞外調(diào)節(jié)蛋白激酶(extracellular regulated protein kinase,ERK)通路激活劑處理或者微RNA-101(microRNA-101,miR-101)抑制子轉(zhuǎn)染后,采用CCK-8和FCM法分別檢測細胞增殖和凋亡情況,采用實時熒光定量PCR和蛋白質(zhì)印跡法檢測細胞中磷酸化ERK(phospho-ERK,p-ERK)、Ras相關(guān)的C3肉毒底物1(Ras-related C3 botulinum toxin substrate 1,Rac1)和miR-101的表達水平。結(jié)果:與正常乳腺上皮細胞相比,乳腺癌細胞中ECT2 mRNA和蛋白的表達水平均明顯升高(P值均0.05)。ECT 2基因沉默后,乳腺癌細胞增殖被明顯抑制(P0.05),細胞凋亡被明顯促進(P0.05),并且細胞中p-ERK和Rac1表達被明顯下調(diào)(P值均0.05),而miR-101表達被明顯上調(diào)(P0.05)。ERK激活劑作用后,ECT2 siRNA轉(zhuǎn)染對p-ERK、miR-101和Rac1表達的影響被明顯反轉(zhuǎn)(P值均0.05);miR-101抑制子轉(zhuǎn)染后,ECT2 siRNA轉(zhuǎn)染對細胞增殖、凋亡以及Rac1表達的影響被反轉(zhuǎn)(P值均0.05),而對p-ERK表達沒有明顯影響(P0.05)。結(jié)論:ECT 2基因沉默可能通過ERK/miR-101/Rac1信號轉(zhuǎn)導通路,調(diào)節(jié)乳腺癌細胞的增殖和凋亡。
[Abstract]:Aim: to investigate the effect of epithelial cell transforming sequence 2 oncogeneECT 2 silencing on the proliferation and apoptosis of breast cancer cells and its potential mechanism. Methods: the expression levels of ECT2 mRNA and protein in normal breast epithelial cells (MCF-10A) and breast cancer cells (MDA-MB-231SK-BR-3MF-7 and BT474) were detected by real-time fluorescence quantitative PCR and Western blot. The specific siRNA(ECT2 siRNAs targeting silenced ECT 2 gene were transfected into breast cancer MDA-MB-231 and MCF-7 cells, then were treated with extracellular regulated protein kinase activator or microRNA-101 miR-101) suppressor transfection. CCK-8 and FCM were used to detect cell proliferation and apoptosis, and real-time fluorescence quantitative PCR and Western blot were used to detect the expression of 1(Ras-related C3 botulinum toxin substrate 1 (Rac1) and miR-101. Results: compared with normal breast epithelial cells, the expression of ECT2 mRNA and protein in breast cancer cells increased significantly after the silencing of 0.05).ECT 2 gene. The proliferation of breast cancer cells was significantly inhibited, the apoptosis was significantly promoted, and the expression of p-ERK and Rac1 were significantly down-regulated (P = 0.05), while the expression of miR-101 was up-regulated by P0.05. ERK activator, and the expression of p-ERKT2-miR-101 and Rac1 was significantly up-regulated by siRNA transfection with ECT2. The proliferation of cells was induced by siRNA transfection of ECT2 siRNA after transfection with 0.05mmiR-101 suppressor. The effect of apoptosis and Rac1 expression was reversed P value was 0.05, but no significant effect on p-ERK expression P0.05. Conclusion the cell proliferation and apoptosis of breast cancer cells may be regulated by ERK/miR-101/Rac1 signal transduction pathway.
【作者單位】： 江西省萍鄉(xiāng)市人民醫(yī)院乳腺外科;
【分類號】：R737.9

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【共引文獻】

相關(guān)期刊論文 前8條

1 肖安;彭蓉蓉;;ECT2基因沉默調(diào)控人乳腺癌細胞增殖和凋亡及其機制探討[J];腫瘤;2017年06期

2 丘s，

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