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首页> 外文期刊>Stem cells international >Cancer Stem Cell Marker Endoglin (CD105) Induces Epithelial Mesenchymal Transition (EMT) but Not Metastasis in Clear Cell Renal Cell Carcinoma
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Cancer Stem Cell Marker Endoglin (CD105) Induces Epithelial Mesenchymal Transition (EMT) but Not Metastasis in Clear Cell Renal Cell Carcinoma

机译：癌症干细胞标志物联结（CD105）诱导上皮间充质转换（EMT）但在透明细胞肾细胞癌中没有转移

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Clear cell renal cell carcinoma (ccRCC) is the most common histological subtype of kidney cancer. We previously reported that CD105(+) subpopulation in human ccRCC tumors possesses tumor cell self-renewal and chemoresistance capability. In this study, we showed that CD105(+) ACHN tumor cells exhibit epithelial mesenchymal transition (EMT) phenotype with high expression of mesenchymal marker N-cadherin and low expression of epithelial marker E-cadherin. They are more motile and invasive compared to the unselected parental ACHN tumor cells. The knockdown of CD105 by RNA interference led to the downregulation of N-cadherin and the upregulation of E-cadherin and reduced motility and invasiveness of CD105(+) cells. Overexpression of stem cell factor MYC in CD105 knocked down cells increased mesenchymal markers and cell motility. However, the CD105(+) population of tumor cells does not exhibit an increase metastatic potential in vivo. Findings from this study support that CD105 plays a functional role in maintaining cancer stem cell and EMT phenotype, with MYC as a common mediator for both of these traits. Our work suggests that the ability to metastasize does not coincide with the cancer stem cell or EMT function of CD105.
机译：透明细胞肾细胞癌（CCRCC）是肾癌最常见的组织学亚型。我们之前报道的是，人类CCRCC肿瘤的CD105（+）亚群具有肿瘤细胞自我更新和化学血容量能力。在这项研究中，我们表明CD105（+）ACHN肿瘤细胞表现出上皮间充质转变（EMT）表型，具有高表达的间充质标记物N-钙粘蛋白和上皮标记物E-Cadherin的低表达。与未选择的父母Achn肿瘤细胞相比，它们更具动机和侵袭性。通过RNA干扰的CD105敲低导致N-Cadherin的下调和e-cadherin的上调和CD105（+）细胞的运动性和侵袭性降低。干细胞因子MyC在CD105中的过度表达撞击细胞增加的间充质标志物和细胞运动性。然而，CD105（+）肿瘤细胞的群体不会在体内提高转移性​​潜力。从该研究支持的结果支持CD105在维持癌症干细胞和EMT表型中起作用的作用，用Myc作为这些性状的常见介体。我们的作品表明，转移的能力与CD105的癌症干细胞或EMT功能不一致。

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