State Key Laboratory of Ultrasound in Medicine and Engineering, College of Biomedical Engineering, Chongqing Medical University, Chongqing, 400016, People's Republic of China.
Molecular Biology Laboratory of Respiratory Disease, Key Laboratory of Clinical Laboratory Diagnostics (Ministry of Education), College of Laboratory Medicine, Chongqing Medical University, Chongqing, 400016, People's Republic of China.
Int J Nanomedicine. 2024 Nov 1;19:11087-11104. doi: 10.2147/IJN.S472796. eCollection 2024.
INTRODUCTION: Inhalation exposure to silica nanoparticles (SiNPs) is frequently inevitable in modern times. Although the impact of SiNPs on the ecological niche of the lungs has been extensively explored, the role and mechanism of SiNPs in the microenvironment of lung tumors remain elusive. METHODS: In this investigation, Lewis lung carcinoma (LLC) was implanted into the left lung in situ after 28 days of intratracheal SiNPs injection into the lungs of mice. This study evaluates the effects of SiNPs on the tumor immune microenvironment both in vitro and in vivo. Our findings indicate that SiNPs can suppress lung cancer by modulating the immune microenvironment of tumors. RESULTS: SiNPs treatment promotes macrophage M1 polarization by activating both NF-κB pathway and glycolytic mechanisms. This phenomenon may be associated with lung inflammation and fluctuation in the pre-metastatic and metastatic microenvironments induced by SiNPs exposure in mice. Additionally, we have shown for the first time that SiNPs have an inhibitory effect on lung carcinogenesis and its progression. CONCLUSION: This study uniquely demonstrates that SiNPs suppress lung cancer by promoting M1 polarization of macrophages in the immune microenvironment of lung tumors. Our findings are critical in exploring the interaction between SiNPs and lung cancer.
简介:在现代,吸入暴露于二氧化硅纳米颗粒(SiNPs)是经常不可避免的。尽管 SiNPs 对肺部生态位的影响已经得到了广泛的研究,但 SiNPs 在肺肿瘤微环境中的作用和机制仍不清楚。
方法:在这项研究中,在向小鼠肺部气管内注射 SiNPs28 天后,将 Lewis 肺癌(LLC)原位植入左肺。本研究评估了 SiNPs 在体外和体内对肿瘤免疫微环境的影响。我们的研究结果表明,SiNPs 通过调节肿瘤的免疫微环境来抑制肺癌。
结果:SiNPs 处理通过激活 NF-κB 途径和糖酵解机制促进巨噬细胞 M1 极化。这种现象可能与 SiNPs 暴露在小鼠中引起的肺部炎症以及前转移和转移微环境的波动有关。此外,我们首次表明,SiNPs 对肺癌的发生和发展具有抑制作用。
结论:这项研究独特地表明,SiNPs 通过促进肺肿瘤免疫微环境中巨噬细胞的 M1 极化来抑制肺癌。我们的研究结果对于探索 SiNPs 与肺癌之间的相互作用至关重要。
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