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首页> 外文期刊>Cytokine >Cellular characteristics of neuroblastoma cells: regulation by the ELR(-)-CXC chemokine CXCL10 and expression of a CXCR3-like receptor.
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Cellular characteristics of neuroblastoma cells: regulation by the ELR(-)-CXC chemokine CXCL10 and expression of a CXCR3-like receptor.

机译：神经母细胞瘤细胞的细胞特征：由ELR（-）-CXC趋化因子CXCL10调控和CXCR3样受体的表达。

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摘要

Bone marrow stroma cells secrete the chemokine CXCL12 that may support bone marrow metastasis formation by neuroblastoma cells. The present study demonstrates that bone marrow stroma cell lines also secrete CXCL10, a chemokine that was shown in the past to have anti-malignancy functions. A receptor recognized by antibodies against CXCR3 was shown to be expressed by six neuroblastoma cell lines. Further detailed analysis was performed on the NUB6 and SK-NMC neuroblastoma cells, showing that CXCL10 induced potent Erk phosphorylation in a G(alphai)-dependent manner. The role of a CXCR3-like receptor in Erk phosphorylation was substantiated by the ability of CXCL11, another potent CXCR3 ligand, to induce Erk phosphorylation in the NUB6 and SK-NMC cells. Further characterization of CXCL10 activities indicated that CXCL10 partly inhibited the growth of the NUB6 and SK-NMC cells. Both NUB6 and SK-NMC cells did not migrate to CXCL10, although their migratory machinery was intact, as evidenced by their migration to bone marrow constituents. Altogether, these results suggest that CXCL10 interacts with a CXCR3-like receptor in neuroblastoma cell lines, raising the possibility that following the homing of the tumor cells to the bone marrow (through a CXCL10-independent mechanism), CXCL10 may partly inhibit neuroblastoma cell growth at this site.
机译：骨髓基质细胞分泌趋化因子CXCL12，它可能支持神经母细胞瘤细胞形成骨髓转移。本研究表明，骨髓基质细胞系还分泌CXCL10，一种过去被证明具有抗恶性功能的趋化因子。已显示由六种成神经细胞瘤细胞系表达被CXCR3抗体识别的受体。在NUB6和SK-NMC神经母细胞瘤细胞上进行了进一步的详细分析，显示CXCL10以Gα依赖性方式诱导有效的Erk磷酸化。 CXCR3样受体在Erk磷酸化中的作用被CXCL11（另一种有效的CXCR3配体）在NUB6和SK-NMC细胞中诱导Erk磷酸化的能力所证实。 CXCL10活性的进一步表征表明，CXCL10部分抑制NUB6和SK-NMC细胞的生长。 NUB6细胞和SK-NMC细胞都没有迁移到CXCL10，尽管它们的迁移机制是完整的，这可以通过迁移到骨髓成分来证明。总而言之，这些结果表明CXCL10与神经母细胞瘤细胞系中的CXCR3样受体相互作用，增加了肿瘤细胞归巢至骨髓后（通过独立于CXCL10的机制），CXCL10可能部分抑制神经母细胞瘤细胞生长的可能性。在这个网站上。

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