Bufalin reduces PD-L1 expression in colorectal cancer cells through suppressing TAM-mediated STAT3 phosphorylation
DOI：10.3872/j.issn.1007-385x.2026.04.003
- VernacularTitle:蟾毒灵通过抑制TAM介导的STAT3磷酸化降低结直肠癌细胞PD-L1表达
- Author:
LU Chang1,2
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SHANG Jing3
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CHEN Jinbao4
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ZHU Yuan2
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ZHONG Jiani2
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YIN Peihao1,5
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Author Information
1. The Fifth Clinical Medical College, Anhui Medical University, Hefei 230022, Anhui, China;
2. Department of General Surgery, Putuo Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai 200062, China;
3. Department of Radiology, Putuo Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai 200062, China;
4. Department of Traditional Chinese Medicine Oncology, Putuo Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai 200062, China;
5. Department of General Surgery, Putuo People's Hospital Affiliated to Tongji University, Shanghai 200061, China
- Publication Type:Journal Article
- Keywords:
结直肠癌；肿瘤相关巨噬细胞；程序性死亡配体1；HCT116细胞
- From:
Chinese Journal of Cancer Biotherapy
2026;33(4):373-378
- CountryChina
- Language:Chinese
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Abstract:
[摘 要] 目的：探讨蟾毒灵（BU）对肿瘤相关巨噬细胞（TAM）介导的结直肠癌（CRC）细胞程序性死亡蛋白-配体1（PD-L1）表达的调控作用及其分子机制。方法：采用HCT116细胞与THP-1来源巨噬细胞构建体外共培养体系。佛波酯（PMA）诱导THP-1细胞分化为M0型巨噬细胞，进一步以HCT116细胞条件培养基（CM）刺激形成TAM样细胞。流式细胞术检测CD11b、CD206表达，以评价巨噬细胞极化水平；RT-qPCR及WB法检测TGF-β、IL-10、STAT3/p-STAT3及PD-L1表达变化；慢病毒转染构建STAT3敲低细胞系HCT116sh-STAT3，结合BU干预验证STAT3/PD-L1信号通路作用。结果：HCT116细胞CM可诱导巨噬细胞向M2表型极化，表现为CD11b⁺CD206⁺细胞比例升高（P < 0.01）及TGF-β、IL-10表达增加（均P < 0.001）。TAM条件培养基可显著促进HCT116细胞STAT3磷酸化（P < 0.001）并上调PD-L1 mRNA及蛋白表达水平（P < 0.001或P < 0.01）。BU干预后，TAM介导的STAT3磷酸化水平明显下降，PD-L1表达同步下调（均P < 0.01）。STAT3敲低可降低PD-L1表达，其作用趋势与BU一致。结论：BU可通过抑制TAM介导的STAT3信号激活，下调CRC细胞PD-L1表达，提示其在肿瘤免疫微环境调控中具有潜在的应用价值。
- Full text:20260521093554934420260403.pdf
