
Histone modifications in cervical cancer: Epigenetic mechanisms, functions and clinical implications (Review)
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- Published online on: August 1, 2025 https://doi.org/10.3892/or.2025.8964
- Article Number: 131
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Copyright: © Li et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
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Abstract
Cervical cancer (CC) poses a substantial global health challenge and it ranks as the fourth most prevalent malignancy among women worldwide. Management strategies include surgical intervention, radiotherapy, chemotherapy and emerging systemic treatments. Although advancements in immunotherapy and targeted therapies have been achieved, the aggressive metastatic nature of the disease, coupled with immune evasion and drug resistance, continues to limit overall survival rates. Therefore, there remains an urgent need to identify novel treatment modalities and more effective therapeutic agents. As fundamental regulators of epigenetic modifications, histone alterations serve a critical role in controlling gene expression, DNA repair mechanisms and cellular differentiation. These modifications include acetylation, methylation, phosphorylation, ubiquitination, ADP‑ribosylation and glycosylation, as well as the more recently identified lactylation and palmitoylation. By restructuring chromatin and facilitating interactions among histones, DNA and regulatory proteins, these modifications exert a substantial influence on cellular functions. Aberrant histone modifications contribute to tumorigenesis, tumor heterogeneity and resistance to conventional anticancer therapies, making them a key focus of oncological research. In recent years, therapeutic strategies targeting histone modifications have gained increasing attention in the treatment of CC. Among these epigenetic alterations, histone acetylation and deacetylation have been extensively studied, with numerous histone deacetylase inhibitors showing promise in preclinical studies. The present review explores the patterns of histone modifications in CC, emphasizing their molecular roles in tumor progression, metastasis and therapeutic resistance. Additionally, histone modification‑driven therapeutic targets are examined, laying the groundwork for future precision medicine approaches in CC treatment.