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Cell-dependent regulation of vasculogenic mimicry by carcinoembryonic antigen cell adhesion molecule 1 (CEACAM1)

机译:癌胚抗原细胞粘附分子1(CEACAM1)对血管生成拟态的细胞依赖性调节

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摘要

Vasculogenic mimicry (VM) promotes tumor migration, metastasis, and invasion in various types of cancer, but the relationship between VM and these phenotypes remains undefined. In this study, we examined carcinoembryonic antigen cell adhesion molecule 1 (CEACAM1) as a novel target of VM. We found that ectopic expression of CEACAM1 in HT1080 human fibrosarcoma cells suppressed the formation of a VM-like network. Further, cell migration and proliferation were abated by the introduction of CEACAM1 into HT1080 cells. Conversely, knockout (KO) of the CEACAM1 gene in SK-MEL-28 melanoma cells, which normally express high levels of CEACAM1, inhibited formation of a VM-like network, which was covered on reintroduction of CEACAM1. These results suggest that CEACAM1 differentially regulates formation of the VM-like network between cancer cell types and implicate CEACAM1 as a novel therapeutic target in malignant cancer.
机译:血管生成模拟(VM)促进各种类型的癌症中的肿瘤迁移,转移和侵袭,但是VM与这些表型之间的关系仍然不确定。在这项研究中,我们检查了癌胚抗原细胞粘附分子1(CEACAM1)作为VM的新型靶标。我们发现在HT1080人纤维肉瘤细胞中异位表达CEACAM1抑制了VM样网络的形成。此外,通过将CEACAM1引入HT1080细胞来减轻细胞迁移和增殖。相反,正常表达高水平CEACAM1的SK-MEL-28黑色素瘤细胞中CEACAM1基因的敲除(KO)抑制了VM样网络的形成,这在重新引入CEACAM1时得到了覆盖。这些结果表明CEACAM1差异调节癌细胞类型之间的VM样网络的形成,并暗示CEACAM1作为恶性肿瘤的新型治疗靶点。

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