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Epigenetic and Post-Translational Modifications in Ferroptosis Regulation and Hepatocellular Carcinoma: New Frontiers in Therapeutic Targeting Publisher Pubmed



Bolandi S ; Dodge S ; Zahed Z ; Soleimani A ; Monirvaghefi K ; Ghodsifar M ; Ghasemi M ; Aghajamal Avval N ; Zadeh S S M ; Fazayel S M A ; Morovatshoar R ; Barfi V ; Behfar Q ; Dehghani S
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Source: Pathology, research and practice Published:2025


Abstract

Hepatocellular carcinoma (HCC), the predominant kind of liver cancer, continues to be a significant contributor to cancer-related deaths globally, influenced by intricate molecular processes and strong resistance to existing chemotherapy. Iron-dependent lipid peroxidation induces ferroptosis, a controlled form of cell death that plays a crucial role in inhibiting tumor growth and treatment resistance in HCC. Recent research has shown that epigenetic modifications, such as DNA methylation, histone modifications, regulation by non-coding RNAs (ncRNAs), and post-translational modification (PTM) like ubiquitination, phosphorylation, acetylation, and methylation, play a crucial role in fine-tuning ferroptosis. These alterations alter the structure of chromatin, gene expression, and protein function, thereby affecting cancer cells' fate. This review emphasizes the complex functions of epigenetic and post-translational alterations in controlling ferroptosis, providing valuable insights into their potential as therapeutic targets in HCC. The unraveling of these pathways offers a significant opportunity for novel therapies targeted at surmounting drug resistance and enhancing patient outcomes in liver cancer. Copyright © 2025. Published by Elsevier GmbH.
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