Desai Parth, Kumari Anjali, Al Abdullah Saqer, Anwar Azreen, Nowlin Kyle, Dellinger Kristen
Department of Nanoscience, Joint School of Nanoscience and Nanoengineering, University of North Carolina at Greensboro, Greensboro, North Carolina, USA.
Department of Nanoengineering, Joint School of Nanoscience and Nanoengineering, North Carolina A&T State University, Greensboro, North Carolina, USA.
Cancer Rep (Hoboken). 2025 Jul;8(7):e70237. doi: 10.1002/cnr2.70237.
Triple-negative breast cancer (TNBC), a leading cause of female mortality worldwide, presents a treatment challenge due to the lack of targeted receptors. Macrophages, recognized for their role in the immune response, provide a promising avenue for cancer research. Given that macrophages secrete extracellular particles (EPs), which have been implicated in biological processes, including intercellular communication and immune modulation, it is hypothesized that EPs derived from macrophages could have potential anticancer effects.
This study examines the effect of M1 macrophage-secreted EPs on TNBC cells to investigate their potential as a therapeutic.
Polarization was induced in RAW 264.7 macrophages and characterized using ELISA, nitrite release, and microscopy. Macrophage-derived EPs were isolated and characterized using nanoparticle tracking analysis, electron microscopy, and western blotting. The influence of EPs on MDA-MB-231 cells, a TNBC model, was assessed using confocal microscopy. Results showed the increasing expression of caspase 3/7 in a time-dependent manner (0, 24, and 48 h). Cell death was observed in TNBC cells with M1 macrophage-derived EPs, while cell proliferation was observed when M2 macrophage-derived EPs interacted with MDA-MB-231 cells.
Overall, results showed that EPs derived from M1 macrophages could induce cell death in MDA-MB-321 cells, opening up potential options for new treatments in TNBC.
三阴性乳腺癌(TNBC)是全球女性死亡的主要原因之一,由于缺乏靶向受体,其治疗面临挑战。巨噬细胞因其在免疫反应中的作用而受到关注,为癌症研究提供了一条有前景的途径。鉴于巨噬细胞分泌细胞外颗粒(EPs),这些颗粒参与包括细胞间通讯和免疫调节在内的生物学过程,因此推测源自巨噬细胞的EPs可能具有潜在的抗癌作用。
本研究检测M1巨噬细胞分泌的EPs对TNBC细胞的影响,以研究其作为一种治疗方法的潜力。
诱导RAW 264.7巨噬细胞极化,并通过酶联免疫吸附测定(ELISA)、亚硝酸盐释放和显微镜检查进行表征。使用纳米颗粒跟踪分析、电子显微镜和蛋白质免疫印迹法对巨噬细胞衍生的EPs进行分离和表征。使用共聚焦显微镜评估EPs对TNBC模型MDA-MB-231细胞的影响。结果显示,半胱天冬酶3/7的表达呈时间依赖性增加(0、24和48小时)。在含有M1巨噬细胞衍生EPs的TNBC细胞中观察到细胞死亡,而当M2巨噬细胞衍生的EPs与MDA-MB-231细胞相互作用时观察到细胞增殖。
总体而言,结果表明源自M1巨噬细胞的EPs可诱导MDA-MB-321细胞死亡,为TNBC的新治疗方法开辟了潜在选择。