通过调节三阴性乳腺癌细胞中的瘤免疫微环境,卡达摩宁具有抗癌作用
Patricia Mendonca1,2, Sukhmandeep Kaur1, Bhonesa Kirpal1
1Division of Pharmaceutical Sciences, College of Pharmacy and Pharmaceutical Sciences, Institute of Public Health, Florida A&M University Tallahassee, FL 32307, The United States.
American journal of cancer research
|January 13, 2025
概括
卡达蒙尼是一种天然化合物,通过调节瘤免疫微环境 (TIME) 和抑制PD-L1表达,在三阴性乳腺癌 (TNBC) 中克服免疫疗法耐药性方面表现有前途.
科学领域:
- 在瘤学瘤学.
- 免疫学 免疫学 免疫学
- 药理学 药理学是指药理学的学科.
背景情况:
- 瘤免疫微环境 (TIME) 对癌症进展和免疫治疗反应至关重要.
- 免疫检查点抑制剂,如PD-1/PD-L1疗法,面临由于新兴耐药性的挑战.
- 需要新的化合物来增强三阴性乳腺癌 (TNBC) 免疫治疗的有效性.
研究的目的:
- 调查天然化合物卡达摩宁对TNBC中PD-L1表达和TIME调节的影响.
- 探索卡达蒙尼在TNBC中克服免疫疗法耐药性的潜力.
主要方法:
- 使用了两个不同的TNBC细胞系:MDA-MB-231和MDA-MB-468.
- 用卡达蒙尼治疗细胞并分析其对PD-L1,JAK1,STAT3,Nrf2,MUC1,NF-κB1,NF-κB2和CCL2水平的影响.
- 评估卡达蒙宁对时间的调制.
主要成果:
- 卡达摩宁抑制了PD-L1表达,并在MDA-231细胞中降低了JAK1/STAT3;在MDA-468细胞中增加了JAK1.
- 卡达摩宁在两种细胞系中都提高了Nrf2的调节,并在MDA-231细胞中降低了MUC1,MDA-468细胞中降低了NF-κB1/2和NF-κB1.
- 卡达蒙尼显著降低了CCL2水平,可能减少巨细胞透,增强T细胞透.
结论:
- 卡达摩宁通过影响TNBC中的关键信号通路和炎症标志物来调节TIME.
- 卡达蒙因降低PD-L1和CCL2的能力表明,它有可能逆转对PD-1/PD-L1免疫疗法的耐药性.
- 卡达摩宁作为TNBC的辅助疗法具有前景,增强免疫疗法结果.
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