Pro-Resolving Mediators in Cancer Inflammation Dynamics

Summary

Inflammation is a double-edged sword in oncology: acute responses defend against malignancy but persistent inflammation fosters tumour initiation, progression and metastasis. Pro-resolving mediators are endogenously produced lipid and peptide autacoids that actively terminate inflammation, restore tissue homeostasis and reprogram immune cells. These mediators derive from polyunsaturated fatty acids and include families such as lipoxins, resolvins, protectins and maresins. In the context of cancer, specialised pro-resolving mediators (SPMs) modulate the tumour microenvironment by attenuating pro-inflammatory cytokines, inhibiting epithelial–mesenchymal transition, limiting angiogenesis and promoting phagocytic clearance of apoptotic cells. By shifting macrophage and neutrophil phenotypes towards resolution, SPMs can enhance antitumour immunity, reduce chemoresistance and potentially improve therapeutic indices. Emerging evidence supports the integration of pro-resolving strategies with conventional therapies, including the use of aspirin-triggered mediators, to achieve dual anti-inflammatory and pro-resolutive effects. This approach holds promise for cancer prevention, adjuvant treatment and mitigation of therapy-induced toxicities, underscoring pro-resolving mediators as a frontier in inflammation-targeted oncology.

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Pro-Resolving Mediators in Cancer Inflammation Dynamics publication trend

The graph below shows the total number of articles in pro-resolving mediators in cancer inflammation dynamics across all publications each year (not limited to Nature Index journals).

Technical terms

Specialised pro-resolving mediators (SPMs): Endogenous lipid and peptide compounds that actively drive resolution of inflammation and restore tissue homeostasis.

Tumour microenvironment (TME): The complex milieu of cancer cells, stromal cells, immune infiltrates, extracellular matrix and signalling molecules surrounding a tumour.

Tumour-associated macrophages (TAMs): Macrophage populations within the TME that can adopt pro-inflammatory or pro-resolving phenotypes influencing tumour progression or regression.

Macrophage polarization: The dynamic process by which macrophages acquire distinct functional states, often described along an inflammatory (M1) to resolving (M2/pro-resolving) spectrum.

Epithelial–mesenchymal transition (EMT): A cellular programme enabling epithelial cancer cells to acquire mesenchymal traits, enhancing invasion and metastatic potential.

References

  1. The Role of Specialized Pro-Resolving Lipid Mediators in Inflammation-Induced Carcinogenesis. International Journal of Molecular Sciences (2023).
  2. Aspirin activates resolution pathways to reprogram T cell and macrophage responses in colitis-associated colorectal cancer. Science Advances (2022).
  3. Resolvin D1 reduces cancer growth stimulating a protective neutrophil-dependent recruitment of anti-tumor monocytes. Journal of Experimental & Clinical Cancer Research (2021).
  4. Specialized Pro-Resolving Mediators Mitigate Cancer-Related Inflammation: Role of Tumor-Associated Macrophages and Therapeutic Opportunities. Frontiers in Immunology (2021).
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