Epithelial mesenchymal transition correlates with CD24+CD44+ and CD133+ cells in pancreatic cancer
Epithelial mesenchymal transition correlates with CD24+CD44+ and CD133+ cells in pancreatic cancer
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DOI：
10.3892/or.2012.1681
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发表时间：
2012-05-01
期刊：
影响因子：
4.2
通讯作者：
Miao, Yi
中科院分区：
文献类型：
--
作者：
Zhang, Ye;Wei, Jishu;Miao, Yi
上皮-间充质转化（EMT）与干细胞样表型的诱导有关，其特征在于细胞表面标志物表达改变和肿瘤形成增加。本研究旨在探讨胰腺癌中EMT与CD 24（+）、CD 44（+）和CD 133（+）细胞的关系。比较未处理和吉西他滨处理的SW 1990吉西他滨耐药细胞和正常SW 1990细胞的形态学。使用siRNA敲低NF-κ B p65表达。免疫印迹法检测Vimentin和E-cadherin的表达，流式细胞仪检测CD 24（+）、CD 44（+）、CD 133（+）细胞的数量。此外，我们还对41例胰腺导管腺癌进行了EMT相关标志物和干细胞相关标志物的免疫组织化学检测。在SW 1990吉西他滨耐药细胞中，与未处理的SW 1990吉西他滨耐药细胞和SW 1990细胞相比，吉西他滨诱导了间充质细胞表型、EMT相关分子标志物的表达以及CD 24（+）、CD 44（+）和CD 133（+）细胞的增加。NF-κ B p65的敲低抑制吉西他滨增加CD 24（+）、CD 44（+）或CD 133（+）细胞比例以及EMT相关分子标志物表达的能力。在人胰腺导管腺癌中，观察到EMT相关标志物波形蛋白和E-钙粘蛋白以及干细胞相关标志物CD 24、CD 133和CD 44的表达之间存在显著相关性。本研究表明胰腺癌中EMT与CD 24（+）、CD 44（+）和CD 133（+）细胞相关。本研究还表明，EMT可能诱导胰腺癌中的癌症干细胞样细胞，不同程度的EMT可能诱导不同比例的CD 24（+）CD 44（+）和CD 133（+）细胞。
The epithelial-mesenchymal transition (EMT) has been linked to induction of a stem-cell like phenotype, characterized by altered cell surface marker expression and increased tumor formation. The aim of this study was to investigate whether EMT correlates with CD24(+)CD44(+) and CD133(+) cells in pancreatic cancer. The morphology of untreated and gemcitabine-treated SW1990 gemcitabine-resistant cells and normal SW 1990 cells were compared. NF-kappa B p65 expression was knocked down using si RNA. Vimentin and E-cadherin expression were analyzed using western blotting, and CD24(+)CD44(+), CD133(+) cells were quantified by FACS. Additionally, immunohistochemistry of EMT-associated markers and stem cell-associated markers were performed in 41 cases of human pancreatic ductal adenocarcinoma. In SW1990 gemcitabine-resistant cells, gemcitabine induced a mesenchymal cell phenotype, expression of EMT-related molecular markers and increased CD24(+)CD44(+) and CD133(+) cells compared to untreated SW 1990 gemcitabine-resistant and SW1990 cells. Knockdown of NF-kappa B p65 inhibited the ability of gemcitabine to increase the proportion of CD24(+)CD44(+) or CD133(+) cells and expression of EMT-related molecular markers. In human pancreatic ductal adenocarcinoma, significant correlations were observed between expression of the EMT-associated markers vimentin and E-cadherin, and stem cell-associated markers CD24, CD133 and CD44. This study demonstrated that EMT correlated with CD24(+)CD44(+) and CD133(+) cells in pancreatic cancer. This study also suggests that EMT may induce cancer stem-like cells in pancreatic cancer, with different degrees of EMT probability inducing different proportions of CD24(+)CD44(+) and CD133(+) cells.