Chouaib S, Noman M Z, Kosmatopoulos K, Curran M A
INSERM (Institut National de la Santé et de la Recherche Médicale) UMR1186, Laboratory «Integrative Tumor Immunology and Genetic Oncology», Villejuif, France.
INSERM, Gustave Roussy, Univ. Paris-Sud, Université Paris-Saclay, Villejuif, France.
Oncogene. 2017 Jan 26;36(4):439-445. doi: 10.1038/onc.2016.225. Epub 2016 Jun 27.
Tumors use several strategies to evade the host immune response, including creation of an immune-suppressive and hostile tumor environment. Tissue hypoxia due to inadequate blood supply is reported to develop very early during tumor establishment. Hypoxic stress has a strong impact on tumor cell biology. In particular, tissue hypoxia contributes to therapeutic resistance, heterogeneity and progression. It also interferes with immune plasticity, promotes the differentiation and expansion of immune-suppressive stromal cells, and remodels the metabolic landscape to support immune privilege. Therefore, tissue hypoxia has been regarded as a central factor for tumor aggressiveness and metastasis. In this regard, manipulating host-tumor interactions in the context of the hypoxic tumor microenvironment may be important in preventing or reverting malignant conversion. We will discuss how tumor microenvironment-driven transient compositional tumor heterogeneity involves hypoxic stress. Tumor hypoxia is a therapeutic concern since it can reduce the effectiveness of conventional therapies as well as cancer immunotherapy. Thus, understanding how tumor and stromal cells respond to hypoxia will allow for the design of innovative cancer therapies that can overcome these barriers. A better understanding of hypoxia-dependent mechanisms involved in the regulation of immune tolerance could lead to new strategies to enhance antitumor immunity. Therefore, discovery and validation of therapeutic targets derived from the hypoxic tumor microenvironment is of major importance. In this context, critical hypoxia-associated pathways are attractive targets for immunotherapy of cancer. In this review, we summarize current knowledge regarding the molecular mechanisms induced by tumor cell hypoxia with a special emphasis on therapeutic resistance and immune suppression. We emphasize mechanisms of manipulating hypoxic stress and its associated pathways, which may support the development of more durable and successful cancer immunotherapy approaches in the future.
肿瘤采用多种策略来逃避宿主免疫反应,包括营造免疫抑制性的不利肿瘤环境。据报道,在肿瘤形成的早期就会因血液供应不足而出现组织缺氧。缺氧应激对肿瘤细胞生物学有强烈影响。特别是,组织缺氧会导致治疗抗性、异质性和进展。它还会干扰免疫可塑性,促进免疫抑制性基质细胞的分化和扩增,并重塑代谢格局以支持免疫豁免。因此,组织缺氧被视为肿瘤侵袭性和转移的核心因素。在这方面,在缺氧肿瘤微环境的背景下操纵宿主与肿瘤的相互作用对于预防或逆转恶性转化可能很重要。我们将讨论肿瘤微环境驱动的短暂组成性肿瘤异质性如何涉及缺氧应激。肿瘤缺氧是一个治疗难题,因为它会降低传统疗法以及癌症免疫疗法的有效性。因此,了解肿瘤和基质细胞如何对缺氧作出反应将有助于设计能够克服这些障碍的创新癌症疗法。更好地理解参与免疫耐受调节的缺氧依赖性机制可能会带来增强抗肿瘤免疫力的新策略。因此,发现和验证源自缺氧肿瘤微环境的治疗靶点至关重要。在这种背景下,关键的缺氧相关途径是癌症免疫治疗的有吸引力的靶点。在本综述中,我们总结了关于肿瘤细胞缺氧诱导的分子机制的当前知识,特别强调治疗抗性和免疫抑制。我们强调操纵缺氧应激及其相关途径的机制,这可能会在未来支持开发更持久、更成功的癌症免疫治疗方法。