Ecto-5'-nucleotidase (CD73) promotes tumor angiogenesis
Ecto-5'-nucleotidase (CD73) promotes tumor angiogenesis
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Ecto-5'-核苷酸酶 (CD73) 促进肿瘤血管生成
DOI：
10.1007/s10585-013-9571-z
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发表时间：
2013-06-01
影响因子：
4
通讯作者：
Shao, Zhimin
中科院分区：
文献类型：
--
作者：
Wang, Li;Tang, Shaoxian;Shao, Zhimin
血管生成在肿瘤的生长、发展和转移中是必不可少的。研究表明，转移性癌中胞外-5 '-核苷酸酶（CD 73）的表达和活性升高。我们前期的研究发现，当肿瘤细胞中的CD 73活性被抑制时，肿瘤移植物的血管生成减少，这意味着该酶参与了肿瘤血管生成。为了阐明其机制，我们研究了CD 73在体外试验和荷瘤小鼠中对肿瘤血管生成的影响。我们发现，在CD 73（+/+）肺微血管内皮细胞（PMEC）中形成的毛细血管样结构比CD 73（-/-）PMEC更多，并且当细胞在癌症条件培养基中培养时更明显。同时，CD 73降低了内皮细胞与IV型胶原的粘附，促进了内皮细胞的迁移。此外，CD 73（+/+）小鼠的肿瘤血管生成程度和肿瘤大小均大于CD 73（-/-）小鼠。因此，我们得出结论，CD 73可以促进内皮细胞在癌症条件下形成新血管，促进肿瘤生长和血行转移。
Angiogenesis is essential for tumor growth, progression and metastasis. Studies indicate that expression and activity of ecto-5'-nucleotidase (CD73) are elevated in metastatic carcinomas. Our previous studies found that angiogenesis of tumor xenografts was decreased when the activity of CD73 in cancer cells was inhibited, implying that this enzyme is involved in tumor angiogenesis. To elucidate the mechanism, we investigated CD73 influence on tumor angiogenesis in both in vitro assays and in tumor bearing mice. We found that capillary-like structures were formed more in CD73(+/+) pulmonary microvascular endothelial cells (PMECs) than CD73(-/-) PMECs, and this was more pronounced when the cells were cultured in cancer-conditioned medium. Meanwhile, CD73 decreased endothelial cells adhesion to collagen IV and promoted migration. Additionally, the extent of tumor angiogenesis and the size of tumors were greater in CD73(+/+) mice than in CD73(-/-) mice. Thus, we concluded that CD73 can promote endothelial cells forming new vessels in cancer condition, facilitating tumor growth and hematogenous metastasis.