The critical role of an inflammatory cytokine IL-1 in tumor microenvironment on regulation of tumor angiogenesis and metastasis

最近，人们强调炎症与肿瘤的进展密切相关。在这项研究中，我们通过比较高表达IL-1α的高转移人肺癌细胞系和低表达IL-1α的低转移肺癌细胞株，证明IL-1通过侵袭表达缺失和淋巴管生成因子的肿瘤支持巨噬细胞，促进肿瘤血管生成和淋巴管生成，导致肺癌细胞的淋巴转移。此外，我们还证明了IL-1/IL-1R靶向药物显著抑制肿瘤血管生成、淋巴管生成和淋巴结转移。因此，IL-1/IL-1R可能在肺癌细胞的恶性进展中起关键作用，而IL-1R靶向药物的治疗效果可能导致另一种治疗淋巴转移的新策略。

Recently it is highlighted that inflammation is closely linked to tumor progression. In this study we demonstrate that IL-1 promotes tumor angiogenesis and lymphangiogenesis through infiltration of tumor supporting macrophages expressing anigogenic and lymphangiogenic factors, resulting in lymph node metastasis of lung cancer cells by comparing highly metastatic human lung cancer cell line expressing higher IL-1alpha with its low metastatic counterpart expressing lower IL-1alpha. Furthermore, we also demonstrate that IL-1/IL-1R-targeted drug significantly suppresses tumor angiogenesis, lymphangiogenesis, and lymph node metastasis. IL-1/IL-1R may thus play crucial roles in malignant progression by lung cancer cells, and the therapeutic efficacy of IL-1R-targeted drugs may lead to an alternative novel strategy to treat lymph node metastasis.