# Association of Chronic Inflammation-Associated Cancer With Cytokines

**Authors:** Hiroshi Nakase, Yuta Shimomori

PMC · DOI: 10.7759/cureus.92239 · 2025-09-13

## TL;DR

This paper reviews how chronic inflammation and cytokines contribute to cancer progression and highlights cytokines as potential targets for cancer treatment.

## Contribution

The paper systematically reviews the role of cytokines in linking chronic inflammation to cancer and emphasizes their therapeutic potential.

## Key findings

- Proinflammatory cytokines like TNF-α, IL-6, and IL-1β promote tumor progression through proliferation and metastasis.
- Anti-inflammatory cytokines such as IL-10 can suppress immune surveillance, aiding tumor growth.
- Targeting cytokine pathways with monoclonal antibodies or inhibitors may reduce tumor-promoting inflammation.

## Abstract

Chronic inflammation supports tissue repair while inadvertently promoting carcinogenesis. Cytokines - critical immune system-signaling molecules - mediate the inflammatory response and establish a cancer-conducive microenvironment. Proinflammatory cytokines, such as tumor necrosis factor-α, interleukin-6, and interleukin-1β, are frequently overexpressed in chronic inflammation and facilitate tumor progression through cell proliferation, survival, angiogenesis, and metastasis. Anti-inflammatory cytokines (e.g., interleukin-10) suppress immune surveillance, which predisposes to tumor growth. Chronic inflammation-induced dysregulation of cytokine networks induces sustained transcriptional factor activation (e.g., nuclear factor-kappa B and signal transducer and activator of transcription 3) that orchestrate gene expression for cell survival and immune evasion. Cytokines influence immune cell recruitment and polarization for immunosuppression and tumor promotion. Emerging evidence highlights the role of cytokines in epithelial-to-mesenchymal transition, a key process in metastasis. Targeting the cytokine-signaling pathway constitutes a promising cancer treatment option. Monoclonal antibodies and small-molecule cytokine inhibitors and their receptors could mitigate tumor-promoting inflammation. Understanding the complex interplay among chronic inflammation, cytokines, and cancer progression is critical for identifying biomarkers and developing targeted therapies to improve clinical outcomes. This review underscores the significance of cytokines in the chronic inflammation-cancer linkage and as potential therapeutic targets. Further research is essential to elucidate intricate cytokine mechanisms in the inflammatory tumor microenvironment for clinical interventions.

## Linked entities

- **Proteins:** IL6 (interleukin 6), IL10 (interleukin 10)
- **Diseases:** cancer (MONDO:0004992)

## Full-text entities

- **Genes:** IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, IL1B (interleukin 1 beta) [NCBI Gene 3553] {aka IL-1, IL1-BETA, IL1F2, IL1beta}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, IL10 (interleukin 10) [NCBI Gene 3586] {aka CSIF, GVHDS, IL-10, IL10A, TGIF}, STAT3 (signal transducer and activator of transcription 3) [NCBI Gene 6774] {aka ADMIO, ADMIO1, APRF, HIES}
- **Diseases:** Cancer (MESH:D009369), Chronic Inflammation (MESH:D007249), metastasis (MESH:D009362), carcinogenesis (MESH:D063646)

## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12517737/full.md

---
Source: https://tomesphere.com/paper/PMC12517737