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Chronic inflammation is a central driver of colorectal cancer initiation and progression, with cytokines and chemokines orchestrating key tumor-promoting processes within the tumor microenvironment. Accumulating evidence indicates that inflammatory mediators—including CCL2, CCL3, CCL5, CXCL1, CCL20, TNF-α, IL-6, IL-8, and TGF-β—contribute to tumor growth, metastasis, immune modulation, and therapeutic resistance. Chemokines regulate immune cell recruitment and stromal remodeling, thereby shaping tumor–immune interactions and influencing disease outcome. Pro-inflammatory cytokines such as TNF-α and IL-6 activate NF-κB and STAT3 signaling pathways, promoting cell survival, angiogenesis, and epithelial–mesenchymal transition (EMT). IL-8 enhances angiogenesis and neutrophil infiltration, while CCL20 and its related signaling networks support cancer stemness and metastatic dissemination. In contrast, TGF-β exhibits context-dependent dual functions, acting as a tumor suppressor in early stages but promoting immune evasion, EMT, and metastasis in advanced disease. This review summarizes the roles of cytokines and chemokines in colorectal cancer progression and highlights their potential as diagnostic biomarkers and therapeutic targets. A deeper understanding of cytokine-mediated signaling networks may provide new opportunities for precision therapy and improved clinical outcomes.
Zhang et al. (Wed,) studied this question.