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首页> 外文期刊>International Journal of Molecular Sciences >Wnt3a Promotes the Vasculogenic Mimicry Formation of Colon Cancer via Wnt/β-Catenin Signaling
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Wnt3a Promotes the Vasculogenic Mimicry Formation of Colon Cancer via Wnt/β-Catenin Signaling

机译：Wnt3a通过Wnt /β-Catenin信号传导促进结肠癌的血管生成拟态形成

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Our previous study provided evidence that non-canonical Wnt signaling is involved in regulating vasculogenic mimicry (VM) formation. However, the functions of canonical Wnt signaling in VM formation have not yet been explored. In this study, we found the presence of VM was related to colon cancer histological differentiation (p 0.001), the clinical stage (p 0.001), and presence of metastasis and recurrence (p 0.001). VM-positive colon cancer samples showed increased Wnt3a expression (p 0.001) and β-catenin nuclear expression (p 0.001) compared with the VM-negative samples. In vitro, over-regulated Wnt3a expression in HT29 colon cancer cells promoted the capacity to form tube-like structures in the three-dimensional (3-D) culture together with increased expression of endothelial phenotype-associated proteins such as VEGFR2 and VE-cadherin. The mouse xenograft model showed that Wnt3a-overexpressing cells grew into larger tumor masses and formed more VM than the control cells. In addition, the Wnt/β-catenin signaling antagonist Dickkopf-1(Dkk1) can reverse the capacity to form tube-like structures and can decrease the expressions of VEGFR2 and VE-cadherin in Wnt3a-overexpressing cells. Taken together, our results suggest that Wnt/β-catenin signaling is involved in VM formation in colon cancer and might contribute to the development of more accurate treatment modalities aimed at VM.
机译：我们之前的研究提供了证据，表明非经典Wnt信号传导参与调节血管生成模拟物（VM）的形成。但是，尚未探讨规范的Wnt信号在VM形成中的功能。在这项研究中，我们发现VM的存在与结肠癌的组织学分化（p <0.001），临床分期（p <0.001）以及转移和复发的存在（p <0.001）有关。与VM阴性样品相比，VM阳性结肠癌样品显示Wnt3a表达增加（p <0.001）和β-catenin核表达（p <0.001）。在体外，HT29结肠癌细胞中Wnt3a表达的过度调节促进了在三维（3-D）培养物中形成管状结构的能力以及与内皮表型相关蛋白（如VEGFR2和VE-钙粘着蛋白）的表达增加。小鼠异种移植模型显示，与对照细胞相比，过量表达Wnt3a的细胞长成更大的肿瘤块并形成更多的VM。此外，Wnt /β-catenin信号传导拮抗剂Dickkopf-1（Dkk1）可以逆转形成管状结构的能力，并可以降低Wnt3a过表达细胞中VEGFR2和VE-钙黏着蛋白的表达。两者合计，我们的结果表明Wnt /β-catenin信号传导参与结肠癌的VM形成，并且可能有助于开发针对VM的更准确的治疗方式。

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