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首页> 外文期刊>Cancer Cell >CXCR2 Inhibition Profoundly Suppresses Metastases and Augments Immunotherapy in Pancreatic Ductal Adenocarcinoma
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CXCR2 Inhibition Profoundly Suppresses Metastases and Augments Immunotherapy in Pancreatic Ductal Adenocarcinoma

机译：CXCR2抑制可显着抑制胰腺导管腺癌的转移和增强免疫治疗。

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摘要

CXCR2 has been suggested to have both tumor-promoting and tumor-suppressive properties. Here we show that CXCR2 signaling is upregulated in human pancreatic cancer, predominantly in neutrophil/myeloid-derived suppressor cells, but rarely in tumor cells. Genetic ablation or inhibition of CXCR2 abrogated metastasis, but only inhibition slowed tumorigenesis. Depletion of neutrophils/myeloid-derived suppressor cells also suppressed metastasis suggesting a key role for CXCR2 in establishing and maintaining the metastatic niche. Importantly, loss or inhibition of CXCR2 improved T cell entry, and combined inhibition of CXCR2 and PD1 in mice with established disease significantly extended survival. We show that CXCR2 signaling in the myeloid compartment can promote pancreatic tumorigenesis and is required for pancreatic cancer metastasis, making it an excellent therapeutic target.
机译：已经建议CXCR2具有促进肿瘤和抑制肿瘤的特性。在这里，我们显示CXCR2信号在人类胰腺癌中上调，主要在中性粒细胞/髓样来源的抑制细胞中，但在肿瘤细胞中很少。遗传消融或抑制CXCR2消除了转移，但只有抑制才减缓了肿瘤的发生。嗜中性粒细胞/髓样来源的抑制细胞的耗竭也抑制了转移，提示CXCR2在建立和维持转移性利基中起关键作用。重要的是，CXCR2的丧失或抑制可改善T细胞的进入，并且在已确诊疾病的小鼠中联合抑制CXCR2和PD1可以显着延长生存期。我们显示，髓系区室中的CXCR2信号传导可以促进胰腺肿瘤发生，并且是胰腺癌转移所必需的，使其成为极好的治疗靶标。

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