Cytokine Mechanisms in Colorectal Cancer Dynamics

The progression of colorectal cancer is intimately shaped by a complex network of cytokines and chemokines that orchestrate tumour growth, immune evasion and metastatic spread. Within the tumour microenvironment, pro-inflammatory mediators such as interleukin-1β, interleukin-6 and tumour necrosis factor-α foster cancer cell proliferation and survival, while chemokines like CXCL8 and CCL20 regulate the recruitment of immune subsets that may either suppress or support the malignancy. Anti-inflammatory signals, including interleukin-10 and transforming growth factor-β, can paradoxically enable tumour escape by dampening cytotoxic T-cell activity or by promoting regulatory T-cell expansion. Systemic cytokine profiles, accessible via peripheral blood sampling, provide prognostic and theranostic insights, revealing signatures that distinguish early and advanced disease. Cross-talk between epithelial cells, stromal fibroblasts and infiltrating leukocytes governs angiogenesis, matrix remodelling and chemoresistance, often via shared pathways such as STAT3 and NF-κB. Emerging evidence highlights cytokine networks as both biomarkers for patient stratification and targets for novel immunomodulatory therapies, underscoring their global significance in improving colorectal cancer outcomes.

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Cytokine Mechanisms in Colorectal Cancer Dynamics publication trend

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

Technical terms

Cytokine: A small protein secreted by immune or tumour cells that modulates inflammation and cell signalling.

Chemokine: A subtype of cytokine specialised in directing the migration of immune cells to sites of inflammation or tumours.

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

Regulatory T cell (Treg): A subset of T lymphocytes that suppress immune responses and may facilitate tumour immune escape.

T helper 17 cell (Th17): An inflammatory T-cell subset producing interleukin-17, implicated in promoting tumour growth and modulating antitumour immunity.

STAT3 signalling: A pathway activated by cytokines that controls gene expression related to cell proliferation, survival and immune regulation.

CXCL8: Also known as interleukin-8, a chemokine that recruits neutrophils and supports angiogenesis within tumours.

CCL20: A chemokine that attracts regulatory T cells and contributes to chemoresistance and immune suppression in colorectal cancer.

References

1. Cytokine-Induced Modulation of Colorectal Cancer. Frontiers in Oncology (2016).
2. Colorectal cancer cell-derived CCL20 recruits regulatory T cells to promote chemoresistance via FOXO1/CEBPB/NF-κB signaling. Journal for ImmunoTherapy of Cancer (2019).
3. Altered expression of cytokines, chemokines, growth factors, and soluble receptors in patients with colorectal cancer, and correlation with treatment outcome. Cancer Immunology, Immunotherapy (2024).
4. Cytokine concentration in peripheral blood of patients with colorectal cancer. Frontiers in Immunology (2023).