The levels of insulin‐like growth factor‐l (IGF‐1) and reactive oxygen species (ROS) are abnormally elevated in various tumour tissues, and IGF‐1 has been reported to be associated with the development and progression of inflammation in cancers. In this study, we found that IGF‐1 activated nuclear factor‐κB (NF‐κB) and NLRP3 inflammatory signalling via IRS‐1/mPGES‐1/NOX2‐regulated ROS. Additionally, in the B16‐F10 tumour‐bearing mouse model, the number of tumours, tumour growth, invasion of tissues and expression of proinflammatory factors in peripheral blood were significantly decreased by treatment with an inhibitor combination compared with those of the IGF‐1 group. Taken together, targeting IRS‐1/mPGES‐1/NOX2 to inhibit inflammation related to NF‐κB and NLRP3 is a potential strategy for controlling the development and progression of cancer.

中文翻译：

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靶向 IRS-1/mPGES-1/NOX2 抑制由胰岛素样生长因子-I 诱导的癌细胞中 NF-κB 和 NLRP3 激活引起的炎症反应。

各种肿瘤组织中胰岛素样生长因子-l (IGF-1) 和活性氧 (ROS) 的水平异常升高，据报道 IGF-1 与癌症炎症的发生和进展有关。在这项研究中，我们发现 IGF-1 通过 IRS-1/mPGES-1/NOX2 调节的 ROS 激活核因子-κB (NF-κB) 和 NLRP3 炎症信号。此外，在 B16-F10 荷瘤小鼠模型中，与 IGF-1 组相比，抑制剂组合治疗后肿瘤数量、肿瘤生长、组织侵袭和外周血促炎因子的表达均显着降低. 总之，靶向 IRS-1/mPGES-1/NOX2 以抑制与 NF-κB 和 NLRP3 相关的炎症是控制癌症发展和进展的潜在策略。