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肿瘤缺氧塑造自然杀伤细胞的抗癌活性。

Tumor hypoxia shapes natural killer cell anticancer activities.

作者信息

Retamal Mauricio A, Salazar-Onfray Flavio, González Fermín E, Tittarelli Andrés

机构信息

Programa de Comunicación en Cáncer, Facultad de Medicina, Instituto de Ciencias E Innovación en Medicina, Clínica Alemana Universidad del Desarrollo, 7610634, Santiago, Chile.

Disciplinary Program of Immunology, Institute of Biomedical Sciences, Faculty of Medicine, Universidad de Chile, 8380453, Santiago, Chile.

出版信息

J Mol Med (Berl). 2025 May 30. doi: 10.1007/s00109-025-02557-6.

Abstract

Tumor hypoxia, a hallmark of the tumor microenvironment (TME), profoundly impacts the antitumor functionality of immune cells, particularly natural killer (NK) cells, which play a critical role in cancer immunosurveillance and immunotherapy success. This review provides a comprehensive analysis of the mechanisms by which hypoxia impairs NK cell-mediated cytotoxicity and antitumor activities, emphasizing the molecular pathways and cellular adaptations that enable cancer cell to evade NK cell attack. Key factors that participate in this phenomenon include the stabilization of hypoxia-inducible factors, metabolic reprogramming, angiogenesis, cancer stemness, autophagy, and the secretion of immunosuppressive molecules. Moreover, hypoxia induces phenotypic and functional changes in both cancer and NK cells, promoting tumor progression and resistance to immunotherapy. Emerging strategies to counteract hypoxia-induced immunosuppression are being explored, including nanotechnology-based approaches, cytokine-mediated NK cell preconditioning, and vascular normalization techniques. These interventions highlight promising avenues for enhancing NK cell functionality and synergizing with existing cancer therapies. By addressing the immunosuppressive challenges of the hypoxic TME, in this review, we underscore the potential of innovative strategies to improve therapeutic outcomes in cancer treatment.

摘要

肿瘤缺氧是肿瘤微环境(TME)的一个标志,深刻影响免疫细胞的抗肿瘤功能,尤其是自然杀伤(NK)细胞,NK细胞在癌症免疫监视和免疫治疗成功中起着关键作用。本综述全面分析了缺氧损害NK细胞介导的细胞毒性和抗肿瘤活性的机制,强调了使癌细胞逃避NK细胞攻击的分子途径和细胞适应性。参与这一现象的关键因素包括缺氧诱导因子的稳定、代谢重编程、血管生成、癌症干性、自噬以及免疫抑制分子的分泌。此外,缺氧会诱导癌细胞和NK细胞的表型和功能变化,促进肿瘤进展和对免疫治疗的抗性。正在探索对抗缺氧诱导的免疫抑制的新策略,包括基于纳米技术的方法、细胞因子介导的NK细胞预处理和血管正常化技术。这些干预措施突出了增强NK细胞功能并与现有癌症疗法协同作用的有前景的途径。通过应对缺氧TME的免疫抑制挑战,在本综述中,我们强调了创新策略在改善癌症治疗疗效方面的潜力。

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