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首页> 外文期刊>Molecular cancer research: MCR >L1-mediated colon cancer cell metastasis does not require changes in EMT and cancer stem cell markers.
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L1-mediated colon cancer cell metastasis does not require changes in EMT and cancer stem cell markers.

机译：L1介导的结肠癌细胞转移不需要EMT和癌症干细胞标志物的改变。

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摘要

Aberrant activation of Wnt/beta-catenin signaling is common in most sporadic and inherited colorectal cancer (CRC) cells leading to elevated beta-catenin/TCF transactivation. We previously identified the neural cell adhesion molecule L1 as a target gene of beta-catenin/TCF in CRC cells. Forced expression of L1 confers increased cell motility, invasion, and tumorigenesis, and the induction of human CRC cell metastasis to the liver. In human CRC tissue, L1 is exclusively localized at the invasive front of such tumors in a subpopulation of cells displaying nuclear beta-catenin. We determined whether L1 expression confers metastatic capacities by inducing an epithelial to mesenchymal transition (EMT) and whether L1 cosegregates with cancer stem cell (CSC) markers. We found that changes in L1 levels do not affect the organization or expression of E-cadherin in cell lines, or in invading CRC tissue cells, and no changes in other epithelial or mesenchymal markers were detected after L1 transfection. The introduction of major EMT regulators (Slug and Twist) into CRC cell lines reduced the levels of E-cadherin and induced fibronectin and vimentin, but unlike L1, Slug and Twist expression was insufficient for conferring metastasis. In CRC cells L1 did not specifically cosegregate with CSC markers including CD133, CD44, and EpCAM. L1-mediated metastasis required NF-kappaB signaling in cells harboring either high or low levels of endogenous E-cadherin. The results suggest that L1-mediated metastasis of CRC cells does not require changes in EMT and CSC markers and operates by activating NF-kappabeta signaling.
机译：Wnt /β-catenin信号转导异常激活在大多数散发性和遗传性结直肠癌（CRC）细胞中很常见，导致β-catenin/ TCF反式激活增加。我们先前将神经细胞粘附分子L1确定为CRC细胞中β-catenin/ TCF的靶基因。 L1的强制表达赋予细胞运动性，侵袭性和肿瘤发生能力，并诱导人CRC细胞向肝脏转移。在人的CRC组织中，L1仅位于显示核β-连环蛋白的细胞亚群中此类肿瘤的侵入性前沿。我们确定L1表达是否通过诱导上皮向间质转化（EMT）赋予转移能力，以及L1是否与癌症干细胞（CSC）标记共分离。我们发现，L1水平的变化不会影响细胞系或侵袭性CRC组织细胞中E-钙粘蛋白的组织或表达，并且在L1转染后未检测到其他上皮或间充质标志物的变化。在CRC细胞系中引入主要的EMT调节剂（Slug和Twist）可降低E-钙粘蛋白水平并诱导纤连蛋白和波形蛋白，但与L1不同，Slug和Twist表达不足以转移。在CRC细胞中，L1没有与CSC标记（包括CD133，CD44和EpCAM）特异性共分离。 L1介导的转移需要内含高水平或低水平内源性E-钙粘着蛋白的细胞中NF-κB信号传导。结果表明，L1介导的CRC细胞转移不需要EMT和CSC标记的变化，并且可以通过激活NF-kappabeta信号进行操作。

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