Modulation of Chronic Cytokine Dysregulation in Cervical Cancer: Potential Biomarkers and Therapeutic Targets

Abstract

Cervical cancer progression is not solely driven by persistent human papillomavirus (HPV) infection but is profoundly influenced by the local immune microenvironment, particularly chronic cytokine imbalances. Unlike the acute cytokine storms observed in infections or sepsis, cervical cancer is characterized by a persistent, low-grade, "smoldering inflammatory response" that fuels tumor initiation, progression, and immune evasion. Pro-inflammatory cytokines such as IL-6, IL-1β, TNF-α, and IL-8 sustain a tumor-supportive milieu, promoting angiogenesis, epithelial-mesenchymal transition, and resistance to apoptosis, while immunosuppressive cytokines like IL-10 and TGF-β dampen anti-tumor immune responses and facilitate immune escape. This review explores chronic cytokine dysregulation in cervical cancer, examining how the prolonged, dysregulated cytokine network shapes the tumor microenvironment, remodels stromal interactions, and influences immune cell recruitment and function. We highlight key cytokines involved in these processes and discuss their clinical significance as potential diagnostic, prognostic, and predictive biomarkers. Understanding these sustained inflammatory processes is critical because they represent a distinct biological landscape compared to acute inflammatory reactions and offer unique windows for therapeutic intervention. The paper reviewed emerging therapeutic strategies targeting these chronic cytokine pathways, including cytokine blockade, immune modulation, and combination approaches integrating immunotherapies or nanomedicine. Addressing chronic cytokine dysregulation holds promise for improving cervical cancer management and patient outcomes.

Keywords: biomarkers; cervical cancer; cytokine storm; inflammation; therapeutic targets.

Figure 1

Cytokine Signaling in Cervical Cancer.

Figure 2

Cytokine- Driven Immune Evasion in Cervical Cancer.

Figure 3

Cytokine Balance in Cervical Cancer Dictates Tumor Fate.