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Abstract

Cervical cancer remains a significant global health burden, particularly in regions with limited access to advanced therapeutics. Beyond viral oncogenesis, accumulating evidence highlights the crucial role of epigenetic dysregulation, particularly KMT2D, in tumor initiation and progression. This literature review aimed to critically synthesize current evidence regarding the biological role of KMT2D in cervical cancer and to explore the opportunities and limitations of antibody-based approaches for future epigenetic intervention. A structured narrative literature review was conducted using PubMed, Scopus, and Web of Science to identify relevant studies published between January 2020 and May 2025. Literature selection was guided by a modified PICO framework and predefined eligibility criteria. The reviewed evidence suggests that KMT2D functions as an important regulator of enhancer activity, chromatin organization, and transcriptional homeostasis in cervical cancer. KMT2D dysregulation has been associated with altered metabolic adaptation, impaired DNA repair pathways, and tumor progression. Current antibody-based applications demonstrate utility primarily in molecular detection and experimental characterization; however, therapeutic translation remains constrained by intracellular delivery barriers and reproducibility challenges. Emerging advances in antibody engineering and intracellular targeting technologies may provide future opportunities to overcome these limitations. KMT2D represents a biologically relevant epigenetic regulator and a potential translational target in cervical cancer.

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