中文摘要：

方面人口(SP ) 房间是从一个有教养的癌症房间孤立的房间的一个小子集衬里癌症干细胞(CSC ) 的类似于那些的那个展览特征，例如变形的高度和 tumorigenic 潜力。产生 SP 房间的恶意的性质的分子的机制不是清楚的。我们从 MCF-7 乳癌房间线孤立 SP 房间并且介绍了 microRNA (miRNA ) 在 SP 导出房间的球状体和 non-SP 房间之间的表示模式。SP 球状体被发现拥有 42 起来调整的 miRNAs 和 27 下面调整的(上面的 5 褶层变化) 。起来调整的 miRNAs 之一， miR-888 计算地预言了参予 adherens 连接(AJ ) 小径，被调查。在 MCF-7 房间的 miR-888 的在表示上减少了为测试被选择的所有四 AJ 小径基因(E-cadherin， ACTG1， PTPRT 和 CDC42 ) 的 mRNA 层次，而将 miR-888 击倒颠倒了趋势。膜 E-cadherin 层次的西方的污点和流动 cytometric quantitation 在这些治疗下面显示出变化的一样的趋势。酶记者试金证明 E-cadherin 是 miR-888 的一个直接目标。作为在恶意的织物建筑学的细胞间的粘着性和维护的一个潜在的角色，结果显示 miR-888 是在 MCF-7 房间的 AJ 小径的一个抑压者并且 miR-888 的起来规定在 MCF-7 SP 房间贡献攻击性。

英文摘要：

Side population （SP） cells are a small subset of cells isolated from a cultured cancer cell line that exhibit characteristics similar to those of cancer stem cells （CSCs）, such as high metastatic and tumorigenic potential. The molecular mechanisms that give rise to the malignant properties of SP cells are not clear. We isolated SP cells from the MCF-7 breast cancer cell line and profiled microRNA （miRNA） expression patterns between SP cell-derived spheroids and non-SP cells. SP spheroids were found to possess 42 up-regulated miRNAs and 27 down-regulated ones （above 5-fold changes）. One of the up-regulated miRNAs, miR-888 computationally predicted to participate in the adherens junction （AJ） pathway, was investigated. Over-expression of miR-888 in MCF-7 cells reduced the mRNA levels of all four AJ pathway genes （E-cadherin, ACTG1, PTPRTand CDC42） that were selected for testing, whereas knocking down miR-888 reversed the trends. Western blot and flow cytometric quantitation of the membrane E-cadherin levels showed the same trend of change under these treatments. Luciferase reporter assay showed E-cadherin is a direct target of miR-888. As a potential role in intercellular adhesiveness and maintenance of malignant tissue architecture, the results indicate that miR-888 is a repressor of the AJ pathway in MCF-7 cells and that up-regulation of miR-888 contributes to aggressiveness in MCF-7 SP cells.