Bakrim Saad, Fessikh Meriem El, Elhrech Hamza, Omari Nasreddine El, Amanullah Mohammed, Ming Long Chiau, Moshawih Said, Bouyahya Abdelhakim
Geo-Bio-Environment Engineering and Innovation Laboratory, Molecular Engineering, Biotechnology and Innovation Team, Polydisciplinary Faculty of Taroudant, Ibn Zohr University, Agadir, 80000, Morocco.
Laboratory of Human Pathologies Biology, Faculty of Sciences, Mohammed V University in Rabat, Rabat, Morocco.
J Transl Med. 2025 May 26;23(1):588. doi: 10.1186/s12967-025-06583-3.
Inflammation is a complex and finely tuned component of the host defense mechanism, responding sensitively to a range of physical, chemical, and biological stressors. Current research is advancing our grasp of both cellular and molecular mechanisms that initiate and regulate interactions within inflammatory pathways. Substantial evidence now indicates a profound link between inflammation, innate immunity, and cancer. Dysregulation of inflammatory pathways is known to be a pivotal factor in the induction, growth, and metastasis of tumors through multiple mechanistic pathways. Basically, the tumor microenvironment (TME), characterized by dynamic interplay between cancerous cells and surrounding inflammatory and stromal cells, plays a central role in these processes. Increasingly, controlled acute inflammation is being explored as a promising therapeutic tool in certain types of cancer. However, inflammatory cells in the TME exhibit remarkable plasticity, with shifting phenotypic and functional roles that facilitate cancer cell survival, proliferation, and migration, especially under chronic inflammatory conditions. Additionally, signaling molecules associated with the innate immune system, like chemokines, are co-opted by malignant cells to support invasion, migration, and metastasis. These findings underscore the need for deeper insights into the mechanisms connecting inflammation to cancer pathology, which could pave the way for innovative diagnostic approaches and targeted anti-inflammatory therapies to counter tumor development. The current review underlines the critical involvement of inflammation in cancer development, examining the connection between the immune system, key inflammatory mediators, biomarkers, and their associated pathways in cancer. We also discuss the impact of inflammation-targeted therapies on anticancer signaling pathways. Furthermore, we review major anti-inflammatory drugs with potential applications in oncology, assessing how inflammation is modulated in cancer management. Lastly, we outline an overview of ongoing discoveries in the field, highlighting both the challenges and the therapeutic promise of targeting inflammation in cancer therapy.
炎症是宿主防御机制中一个复杂且精细调节的组成部分,对一系列物理、化学和生物应激源做出敏感反应。当前的研究正在加深我们对启动和调节炎症途径内相互作用的细胞和分子机制的理解。现在大量证据表明炎症、先天免疫和癌症之间存在着深刻的联系。已知炎症途径的失调是肿瘤诱导、生长和转移过程中通过多种机制途径的关键因素。基本上,以癌细胞与周围炎症细胞和基质细胞之间的动态相互作用为特征的肿瘤微环境(TME)在这些过程中起着核心作用。越来越多的研究开始探索可控的急性炎症作为某些类型癌症的一种有前景的治疗工具。然而,TME中的炎症细胞表现出显著的可塑性,其表型和功能角色不断变化,这有助于癌细胞的存活、增殖和迁移,尤其是在慢性炎症条件下。此外,与先天免疫系统相关的信号分子,如趋化因子,被恶性细胞利用来支持侵袭、迁移和转移。这些发现强调了深入了解将炎症与癌症病理联系起来的机制的必要性,这可能为创新的诊断方法和靶向抗炎疗法以对抗肿瘤发展铺平道路。本综述强调了炎症在癌症发展中的关键作用,研究了免疫系统、关键炎症介质、生物标志物及其在癌症中的相关途径之间的联系。我们还讨论了针对炎症的疗法对抗癌信号通路的影响。此外,我们回顾了在肿瘤学中具有潜在应用的主要抗炎药物,评估了在癌症管理中炎症是如何被调节的。最后,我们概述了该领域正在进行的发现,强调了在癌症治疗中靶向炎症的挑战和治疗前景。