review · Journal of Translational Medicine
Inflammation is closely linked to innate immunity and plays a central role in cancer development. Dysregulated inflammatory pathways drive tumour induction, growth, and metastasis, largely through complex interactions within the tumour microenvironment. While controlled acute inflammation shows promise as an anticancer strategy in specific cancers, chronic inflammation and the plasticity of inflammatory cells often support cancer cell survival, invasion, and spread. Malignant cells also exploit innate immune signalling molecules, including chemokines, to advance metastatic progression. Targeting these inflammatory mechanisms offers pathways for novel diagnostics and oncology treatments. Major anti-inflammatory medicines present therapeutic possibilities for modulating these pathways in cancer care, although functional shifts among inflammatory cells in the tumour microenvironment continue to pose therapeutic challenges.
Understanding how the immune system and inflammation influence tumour biology is essential for creating more effective cancer treatments. Chronic inflammation often shields tumours and assists their spread, whereas controlled acute inflammation can fight malignant cells. Unravelling these mechanisms helps guide the repurposing of existing anti-inflammatory drugs and the development of targeted therapies that block tumour progression.
This research informs the development of targeted anti-inflammatory cancer therapies and diagnostic biomarkers. Potential end users include pharmaceutical developers and clinical oncologists looking to repurpose existing anti-inflammatory drugs or design targeted interventions that disrupt tumour-promoting inflammation. Because the evidence derives from a broad review of mechanisms and therapeutic concepts, commercial translation remains at an early discovery and exploratory stage.
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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.
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DOI: 10.1186/s12967-025-06583-3
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