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首页> 外文期刊>Progress in Artificial Intelligence >Interleukin-22 Mediates the Chemotactic Migration of Breast Cancer Cells and Macrophage Infiltration of the Bone Microenvironment by Potentiating S1P/SIPR Signaling
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Interleukin-22 Mediates the Chemotactic Migration of Breast Cancer Cells and Macrophage Infiltration of the Bone Microenvironment by Potentiating S1P/SIPR Signaling

机译：白细胞介素-22通过增强S1P / SIPR信号传导介导乳腺癌细胞的嗜嗜癌细胞和巨噬细胞渗透的嗜嗜癌迁移

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摘要

The interleukin-22 (IL-22) signaling pathway is well known to be involved in the progression of various cancer types but its role in bone metastatic breast cancer remains unclear. We demonstrate using human GEO profiling that bone metastatic breast cancer displays elevated interleukin-22 receptor 1 (IL-22R1) and sphingosine-1-phosphate receptor 1 (S1PR1) expression. Importantly, IL-22 stimuli promoted the expression of IL-22R1 and S1PR1 in aggressive MDA-MB-231 breast cancer cells. IL-22 treatment also increased sphingosine-1-phosphate production in mesenchymal stem cells (MSCs) and induced the sphingosine-1-phosphate (S1P)-mediated chemotactic migration of MDA-MB-231 cells. This effect was inhibited by an S1P antagonist. In addition to the S1PR1 axis, IL-22 stimulated the expression of matrix metalloproteinase-9 (MMP-9), thereby promoting breast cancer cell invasion. Moreover, IL-22 induced IL22R1 and S1PR1 expression in macrophages, myeloid cell, and MCP1 expression in MSCs to facilitate macrophage infiltration. Immunohistochemistry indicated that IL-22R1 and S1PR1 are overexpressed in invasive malignant breast cancers and that this correlates with the MMP-9 levels. Collectively, our present results indicate a potential role of IL-22 in driving the metastasis of breast cancers into the bone microenvironment through the IL22R1-S1PR1 axis.
机译：白细胞介素-22（IL-22）信号传导途径众所周知，涉及各种癌症类型的进展，但其在骨转移乳腺癌中的作用仍不清楚。我们用人的地理概况证明骨转移性乳腺癌显示升高的白细胞介素-22受体1（IL-22R1）和鞘氨醇-1-磷酸受体1（S1PR1）表达。重要的是，IL-22刺激促进IL-22R1和S1PR1在侵蚀性MDA-MB-231乳腺癌细胞中的表达。 IL-22治疗还增加了间充质干细胞（MSCs）的鞘氨氨酸-1-磷酸盐产生，并诱导了MDA-MB-231细胞的鞘氨氨酸-1-磷酸酯（S1P）介导的趋化迁移。 S1P拮抗剂抑制了这种效果。除了S1PR1轴外，IL-22刺激了基质金属蛋白酶-9（MMP-9）的表达，从而促进乳腺癌细胞侵袭。此外，IL-22诱导巨噬细胞，骨髓细胞和MCP1表达的IL-22诱导IL22R1和S1PR1表达，以促进巨噬细胞浸润。免疫组织化学表明IL-22R1和S1PR1在侵袭性恶性乳腺癌中过表达，并且这种与MMP-9水平相关。集体，我们的目前的结果表明IL-22通过IL22R1-S1PR1轴将乳腺癌转移到骨微环境中的潜在作用。

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