Zheng Wei, Wang Yuxin, Sun Haoyang, Bao Surina, Ge Shuai, Quan Chunshan
Key Laboratory of Biotechnology and Bioresources Utilization of Ministry of Education, College of Life Science, Dalian Minzu University, Dalian, China.
Department of Bioengineering, College of Life Science, Dalian Minzu University, Dalian, Liaoning, China.
Front Immunol. 2025 Apr 3;16:1549564. doi: 10.3389/fimmu.2025.1549564. eCollection 2025.
is strongly linked to colorectal cancer (CRC) progression, but its mechanisms for influencing macrophage polarization and tumor development are not well understood. We established an model of infection in RAW264.7 macrophages to investigate these processes. Macrophage polarization was evaluated using scanning electron microscopy (SEM), real-time quantitative PCR (RT-qPCR), and immunofluorescence staining. RNA sequencing (RNA-Seq) identified differentially expressed genes (DEGs) and enriched pathways, focusing on the role of the NF-κB signaling pathway in macrophage polarization. infection induced M2 polarization in RAW264.7 macrophages, as confirmed by SEM analysis and RT-qPCR validation. A total of 2,029 DEGs were identified after infection, with 763 upregulated and 1,266 downregulated. GO and KEGG enrichment analysis showed that cytokine-cytokine receptor interaction, TNF signaling, and NF-κB signaling pathways are upregulated in macrophages after infection, indicating enhanced cytokine activity and immune response. Key genes (, , , , , ) and proteins (P50, P100) in the NF-κB pathway are upregulated, indicating the crucial role of the NF-κB pathway in M2 macrophage polarization. This study offers crucial evidence regarding the role of the NF-κB signaling pathway in modulating -induced macrophage M2 polarization, underscoring its significance in the progression of colorectal cancer.
与结直肠癌（CRC）进展密切相关，但其影响巨噬细胞极化和肿瘤发展的机制尚不清楚。我们在RAW264.7巨噬细胞中建立了感染模型以研究这些过程。使用扫描电子显微镜（SEM）、实时定量PCR（RT-qPCR）和免疫荧光染色评估巨噬细胞极化。RNA测序（RNA-Seq）鉴定了差异表达基因（DEGs）和富集途径，重点关注NF-κB信号通路在巨噬细胞极化中的作用。感染诱导RAW264.7巨噬细胞发生M2极化，这通过SEM分析和RT-qPCR验证得到证实。感染后共鉴定出2029个DEGs，其中763个上调，1266个下调。GO和KEGG富集分析表明，感染后巨噬细胞中细胞因子-细胞因子受体相互作用、TNF信号和NF-κB信号通路上调，表明细胞因子活性和免疫反应增强。NF-κB通路中的关键基因（、、、、、）和蛋白质（P50、P100）上调，表明NF-κB通路在M2巨噬细胞极化中起关键作用。本研究提供了关于NF-κB信号通路在调节诱导的巨噬细胞M2极化中的作用的关键证据，强调了其在结直肠癌进展中的重要性。
