| 殷晋伟,汤建磊,许姣.基于生物信息学分析白细胞介素 -33在非小细胞肺癌中的表达及验证[J].安徽医药,2026,30(10):1991-1997. |
| 基于生物信息学分析白细胞介素 -33在非小细胞肺癌中的表达及验证 |
| Expression and validation of IL-33 in non-small cell lung cancer based on bioinformatics analysis |
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| DOI：10.3969/j.issn.1009-6469.2026.10.016 |
| 中文关键词: 白细胞介素 -33 癌，非小细胞肺 生物信息学 肿瘤转移 肺癌分期 肺癌预后 |
| 英文关键词: Interleukin-33 Carcinoma,non-small-cell lung cancer prognosis |
| 基金项目:江苏省检验医学重点实验室开放课题项目( JSKLM-Y-2025-03)；常州市卫生健康委重大项目( ZD202455)；常州市卫生健康青苗人才培养工程项目( CZQM2021025)；徐州医科大学附属医院发展基金优秀人才基金项目( XYFY202305) |
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| 中文摘要: |
| 目的分析白细胞介素(IL)-33在非小细胞肺癌( non-small cell lung cancer，NSCLC)中的表达及促进 NSCLC增殖和转移的可能机制。方法通过癌症基因组图谱( the cancer genome atlas，TCGA)和基因表达综合数据库( gene expression omnibus， GEO)等在线网站获得 IL-33表达数据，结合 NSCLC病人生存资料分析 IL-33在 NSCLC中的表达及促进 NSCLC的增殖和转移分子生物学机制。选取 2018年 1月至 2023年 12月在无锡市锡山人民医院和江苏大学附属武进医院经病理组织学确诊为 NSCLC的 50例病人为研究对象，选择癌旁组织作为对照(正常组)；采用免疫组织化学染色和蛋白质印迹法检测肺癌组织标本中 IL-33的表达。结果免疫荧光结果显示肺鳞癌、腺癌组中 IL-33高表达，且 IL-33high，IL-33Med和 IL-33Low的表达差异有统计学意义( F=17.15，P=0.011)；蛋白质印迹法证明，与癌旁组织(正常组)相比，肺鳞癌、腺癌组中高表达 IL-33蛋白( P<0.01)。 NSCLC癌组织中 IL-33的表达与肿瘤的 TNM分期相关，差异有统计学意义( χ2=4.33，P=0.038)但与年龄、性别、吸烟及肿瘤的组织学类型差异无统计学意义( P>0.05)。生物信息学分析显示 IL-33在 NSCLC中显著高表达，，且随着肿瘤 -淋巴结 -转移分期系统分期呈现先下降后上升的趋势( P<0.05)；在Ⅲ~Ⅳ期病人肿瘤中， IL-33的恢复表达与该阶段肿瘤更加活跃的远端转移相关； IL-33高表达 NSCLC病人生存期较 IL-33低表达者显著缩短(P<0.05)； CancerSEA数据库分析结果显示， IL-33在肺腺癌中发挥促癌的功能，与血管生成和 IL-1受体 1型、髓样分化因子 88、IL-1受体辅助蛋白等多种蛋白介导的炎症反应密切相关；肿瘤免疫浸润分析资源库数据库显示，肺腺癌中 IL-33和 CD8+T细胞浸润密切相关，肺鳞癌中 IL-33和巨噬细胞浸润密切相关； IL-33与微卫星不稳定性、肿瘤突变负荷密切相关； KOBAS数据库提示， IL-33通过 TCR信号、细胞因子、免疫反应、 PD1/PDL1、TGF-β和上游调控的 miRNA通路等促进 NSCLC的发生发展。结论 IL-33在 NSCLC肿瘤中呈现高表达，可通过多种调控途径发挥促进 NSCLC发生发展的作用。 |
| 英文摘要: |
| Objective To investigate the expression of interleukin-33 (IL-33) in non-small cell lung cancer (NSCLC) and the poten-tial mechanisms by which it promotes NSCLC proliferation and metastasis.Methods IL-33 expression data were obtained from onlinedatabases including The Cancer Genome Atlas (TCGA) and the Gene Expression Omnibus (GEO), and combined with survival data of NSCLC patients to analyze IL-33 expression and its molecular biological roles in NSCLC. A total of 50 patients with histopathologicallyconfirmed NSCLC treated at Wuxi Xishan People's Hospital and Wujin Hospital Affiliated to Jiangsu University from January 2018 toDecember 2023 were enrolled, with adjacent non-tumor tissues serving as normal controls. Immunofluorescence and Western blotting were performed to detect IL-33 expression in lung cancer tissue specimens.Results Immunofluorescence showed high IL-33 expres-sion in lung squamous cell carcinoma and adenocarcinoma, with statistically significant differences among the IL-33-high, IL-33-medi-um, and IL-33-low expression groups (F=17.15, P=0.011). Western blotting confirmed that IL-33 protein expression was significantly upregulated in NSCLC tissues compared with adjacent non-tumor tissues (P<0.01). IL-33 expression in NSCLC tissues was associated with TNM stage, with statistically significant difference (χ2=4.33, P=0.038), but showed no significant correlations with age, sex, smok-ing status, or histological type (P>0.05). Bioinformatics analysis revealed that IL-33 was significantly overexpressed in NSCLC, with a trend of initially decreasing and then increasing across TNM stages (P<0.05). In patients with stage Ⅲ-Ⅳ disease, the restored expres-sion of IL-33 was associated with more active distant metastasis at this stage. NSCLC patients with high IL-33 expression had signifi-cantly shorter survival than those with low IL-33 expression (P<0.05). Analysis using the CancerSEA database indicated that IL-33 ex-erted oncogenic functions in lung adenocarcinoma, closely associated with angiogenesis and inflammatory responses mediated by pro-teins such as interleukin-1 receptor type 1, myeloid differentiation factor 88, and interleukin-1 receptor accessory protein. The Tumor Immune Estimation Resource (TIMER) database demonstrated that IL-33 expression was closely correlated with CD8. T-cell infiltration in lung adenocarcinoma and with macrophage infiltration in lung squamous cell carcinoma. IL-33 was also closely associated with mic-rosatellite instability and tumor mutational burden. KOBAS database analysis suggested that IL-33 promoted NSCLC progression through pathways including T-cell receptor signaling, cytokine-mediated responses, immune regulation, the PD-1/PD-L1 axis, TGF-β signaling, and upstream miRNA-mediated regulatory networks.Conclusion IL-33 is highly expressed in NSCLC and may promote the development and progression of NSCLC through multiple regulatory pathways. |
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