D'Urso Annarita, Oltolina Francesca, Borsotti Chiara, Prat Maria, Colangelo Donato, Follenzi Antonia
Department of Health Sciences, School Medicine, Università del Piemonte Orientale A. Avogadro, Via Solaroli 17, 28100 Novara, Italy.
Pharmaceutics. 2023 Jun 12;15(6):1711. doi: 10.3390/pharmaceutics15061711.
New therapeutic strategies are required in cancer therapy. Considering the prominent role of tumor-associated macrophages (TAMs) in the development and progression of cancer, the re-education of TAMs in the tumor microenvironment (TME) could represent a potential approach for cancer immunotherapy. TAMs display an irregular unfolded protein response (UPR) in their endoplasmic reticulum (ER) to endure environmental stress and ensure anti-cancer immunity. Therefore, nanotechnology could be an attractive tool to modulate the UPR in TAMs, providing an alternative strategy for TAM-targeted repolarization therapy. Herein, we developed and tested polydopamine-coupled magnetite nanoparticles (PDA-MNPs) functionalized with small interfering RNAs (siRNA) to downregulate the protein kinase R (PKR)-like ER kinase (PERK) expression in TAM-like macrophages derived from murine peritoneal exudate (PEMs). After the evaluation of the cytocompatibility, the cellular uptake, and the gene silencing efficiency of PDA-MNPs/siPERK in PEMs, we analyzed their ability to re-polarize in vitro these macrophages from M2 to the M1 inflammatory anti-tumor phenotype. Our results indicate that PDA-MNPs, with their magnetic and immunomodulator features, are cytocompatible and able to re-educate TAMs toward the M1 phenotype by PERK inhibition, a UPR effector contributing to TAM metabolic adaptation. These findings can provide a novel strategy for the development of new tumor immunotherapies in vivo.
癌症治疗需要新的治疗策略。考虑到肿瘤相关巨噬细胞(TAM)在癌症发生和发展中的突出作用,对肿瘤微环境(TME)中的TAM进行重新编程可能是癌症免疫治疗的一种潜在方法。TAM在内质网(ER)中表现出不规则的未折叠蛋白反应(UPR),以承受环境压力并确保抗癌免疫。因此,纳米技术可能是调节TAM中UPR的一种有吸引力的工具,为TAM靶向的再极化治疗提供了另一种策略。在此,我们开发并测试了用小干扰RNA(siRNA)功能化的聚多巴胺偶联磁铁矿纳米颗粒(PDA-MNP),以下调源自小鼠腹腔渗出液(PEM)的TAM样巨噬细胞中蛋白激酶R(PKR)样内质网激酶(PERK)的表达。在评估了PDA-MNP/siPERK在PEM中的细胞相容性、细胞摄取和基因沉默效率后,我们分析了它们在体外将这些巨噬细胞从M2重新极化为M1炎症抗肿瘤表型的能力。我们的结果表明,具有磁性和免疫调节特性的PDA-MNP具有细胞相容性,并且能够通过抑制PERK(一种有助于TAM代谢适应的UPR效应器)将TAM重新编程为M1表型。这些发现可以为体内新的肿瘤免疫治疗的开发提供一种新策略。