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CEACAM1 可形成支持肿瘤血管成熟的促血管生成肿瘤微环境。

CEACAM1 creates a pro-angiogenic tumor microenvironment that supports tumor vessel maturation.

机构信息

Institute of Clinical Chemistry, Center for Diagnostics, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.

出版信息

Oncogene. 2011 Oct 13;30(41):4275-88. doi: 10.1038/onc.2011.146. Epub 2011 May 2.

Abstract

We have studied the effects of carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) on tumor angiogenesis in murine ductal mammary adenocarcinomas. We crossed transgenic mice with whey acidic protein promoter-driven large T-antigen expression (WAP-T mice) with oncogene-induced mammary carcinogenesis with CEACAM1null mice, and with Tie2-Ceacam1 transgenics, in which the Tie2 promoter drives endothelial overexpression of CEACAM1 (WAP-T × CEACAM1(endo+) mice), and analyzed tumor vascularization, angiogenesis and vessel maturation in these mice. Using flat-panel volume computed tomography (fpVCT) and histology, we found that WAP-T × CEACAM1(endo+) mice exhibited enhanced tumoral vascularization owing to CEACAM1(+) vessels in the tumor periphery, and increased intratumoral angiogenesis compared with controls. In contrast, vascularization of CEACAM1null/WAP-T-derived tumors was poor, and tumor vessels were dilated, leaky and showed poor pericyte coverage. Consequently, the tumoral vasculature could not be visualized in CEACAM1null/WAP-T mice by fpVCT, and we observed poor organization of the perivascular extracellular matrix (ECM), accompanied by the accumulation of collagen IV-degrading matrix metalloproteinase 9(+) (MMP9(+)) leukocytes and stromal cells. Vascular instability and alterations in ECM structure were accompanied by a significant increase in pulmonary metastases in CEACAM1null/WAP-T mice, whereas only occasional metastases were observed in CEACAM1(+) hosts. In CEACAM1(+) hosts, intratumoral vessels did not express CEACAM1, but they were intact, extensively covered with pericytes and framed by a well-organized perivascular ECM. MMP9(+) accessory cells were largely absent. Orthotopic transplantation of primary WAP-T- and CEACAM1null/WAP-T tumors into all three mouse lines confirmed that a CEACAM1(+) host environment is a prerequisite for productive angiogenic remodeling of the tumor microenvironment. Hence, CEACAM1 expression in the tumor periphery determines the vascular phenotype in a tumor, whereas systemic absence of CEACAM1 interferes with the formation of an organized tumor matrix and intratumoral vessel maturation.

摘要

我们研究了癌胚抗原相关细胞黏附分子 1(CEACAM1)对小鼠乳腺导管腺癌肿瘤血管生成的影响。我们将乳清酸性蛋白启动子驱动大 T 抗原表达的转基因小鼠(WAP-T 小鼠)与致癌基因诱导的乳腺肿瘤发生与 CEACAM1null 小鼠,以及与 Tie2-Ceacam1 转基因小鼠(其中 Tie2 启动子驱动内皮细胞 CEACAM1 过表达,WAP-T×CEACAM1(endo+)小鼠)进行杂交,并分析这些小鼠的肿瘤血管生成、血管生成和血管成熟。使用平板容积 CT(fpVCT)和组织学,我们发现 WAP-T×CEACAM1(endo+)小鼠由于肿瘤周边的 CEACAM1(+)血管而表现出增强的肿瘤血管生成,并且与对照组相比,肿瘤内血管生成增加。相比之下,CEACAM1null/WAP-T 衍生肿瘤的血管生成较差,肿瘤血管扩张、渗漏且周细胞覆盖不良。因此,fpVCT 无法在 CEACAM1null/WAP-T 小鼠中可视化肿瘤血管,并且我们观察到血管周围细胞外基质(ECM)的组织不良,伴随着胶原 IV 降解的基质金属蛋白酶 9(MMP9(+))白细胞和基质细胞的积累。血管不稳定和 ECM 结构改变伴随着 CEACAM1null/WAP-T 小鼠肺部转移的显著增加,而在 CEACAM1(+)宿主中仅观察到偶尔的转移。在 CEACAM1(+)宿主中,肿瘤内血管不表达 CEACAM1,但它们完整,被大量周细胞覆盖,并被组织良好的血管周围 ECM 包围。MMP9(+)辅助细胞大部分不存在。将原发性 WAP-T 和 CEACAM1null/WAP-T 肿瘤原位移植到所有三种小鼠系中证实,CEACAM1(+)宿主环境是肿瘤血管生成重塑的必要条件。因此,肿瘤周边的 CEACAM1 表达决定了肿瘤的血管表型,而系统性缺乏 CEACAM1 会干扰有组织的肿瘤基质形成和肿瘤内血管成熟。

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