Epigenetic Modifiers as Therapeutic Targets at the Interface of Infectious Diseases and Cancer Progression

Abstract

Epigenetic regulation plays a central role in controlling gene expression programs that govern cellular identity, immune responses, and adaptation to environmental stress. Increasing evidence demonstrates that dysregulation of epigenetic mechanisms is a shared hallmark of both infectious diseases and cancer progression, enabling pathogen persistence, immune evasion, malignant transformation, and therapeutic resistance. Epigenetic modifiers—including DNA methyltransferases, histone-modifying enzymes, chromatin remodelers, and non-coding RNAs—mediate reversible yet stable transcriptional changes that bridge genetic predisposition and environmental influence. In infectious diseases, pathogens actively exploit host epigenetic machinery to suppress antimicrobial responses and establish chronic or latent infections, while host-directed epigenetic reprogramming can shape immune memory and disease outcomes. In cancer, aberrant epigenetic landscapes drive silencing of tumor suppressor genes, maintenance of cancer stem cell plasticity, and resistance to cytotoxic and immune-based therapies. Importantly, the reversibility of epigenetic alterations has enabled the clinical development of epigenetic drugs, particularly in oncology, and has opened new avenues for therapeutic repurposing in infectious diseases, although challenges related to target specificity, context-dependent effects, and potential toxicity continue to limit their broader clinical application. This review provides an integrative overview of epigenetic regulation in health and disease, examines the role of epigenetic modifiers in host–pathogen interactions and cancer progression, and highlights emerging translational strategies, including combination therapies and epigenome editing technologies. By bridging insights from infectious disease biology and cancer research, this work underscores the potential of epigenetic modifiers as unifying and versatile therapeutic targets in complex human diseases.