Cytokine Signaling in Cancer and Inflammation

Cytokines are soluble mediators that orchestrate cell-to-cell communication in both immune surveillance and pathological processes. In cancer, aberrant cytokine networks foster tumour initiation, progression and metastasis by modulating proliferation, survival, angiogenesis and the tumour microenvironment. Chronic inflammatory conditions often precede or accompany malignancy, with cytokines such as interleukin-6 family members activating JAK/STAT, MAPK and NF-κB cascades to sustain a pro-tumour milieu. Conversely, dysregulated cytokine signalling underlies tissue injury and fibrotic remodelling in cardiovascular, gastrointestinal and other inflammatory diseases. Recent advances have elucidated receptor heterodimerisation, downstream kinase activation and transcriptional control as critical nodes that integrate diverse stimuli. Therapeutic strategies targeting cytokine receptors, associated kinases and feedback inhibitors are now entering clinical development, offering promise for both anti-inflammatory and anti-cancer interventions.

Research from Nature Portfolio

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Cytokine Signaling in Cancer and Inflammation publication trend

The graph below shows the total number of articles in cytokine signaling in cancer and inflammation across all publications each year (not limited to Nature Index journals).

Technical terms

Cytokine: A small secreted protein that mediates intercellular communication in immune responses and tissue homeostasis.

JAK/STAT pathway: A signal transduction cascade activated by cytokine receptors leading to phosphorylation of STAT transcription factors.

NF-κB: A transcription factor complex that regulates genes involved in inflammation, immunity and cell survival.

Chemoresistance: The ability of cancer cells to withstand the effects of chemotherapy through molecular adaptations.

Macrophage polarisation: The process by which macrophages adopt distinct functional phenotypes in response to environmental cues.

PI3K/Akt pathway: A kinase signalling axis that controls cell growth, metabolism and survival in response to extracellular stimuli.

References

1. Blocking Oncostatin M receptor abrogates STAT3 mediated integrin signaling and overcomes chemoresistance in ovarian cancer. npj Precision Oncology (2024).
2. OSMR deficiency aggravates pressure overload-induced cardiac hypertrophy by modulating macrophages and OSM/LIFR/STAT3 signalling. Journal of Translational Medicine (2023).
3. Hydrogen Sulfide Downregulates Oncostatin M Expression via PI3K/Akt/NF-κB Signaling Processes in Neutrophil-like Differentiated HL-60 Cells. Antioxidants (2023).