Abstract

Currently, traditional cancer therapy still falls far short of expectations. However, a variety of invasive cancers that are resistant to chemotherapy (such as platinum drugs, one of the most applied antineoplastics in clinic) and targeted agents are susceptible to ferroptosis. Ferroptosis is a form of cell death that is driven by cell metabolism and iron-dependent lipid peroxidation. Ferroptosis inducers can eliminate the drug resistance of tumor cells in the mesenchymal state, effectively inhibit the drug resistance of acquired tumor cells, and optimize cancer efficacy. Research based on the epigenetic mechanism of ferroptosis is still in the stage of screening and verifying the regulatory effect, and there is no complete regulatory mechanism network. In this review, we expound on the epigenetic regulation and nonepigenetic mechanisms of ferroptosis and review the epigenetic-based mechanisms of tumor therapy potential and emerging nonepigenetic-based therapies (nanotherapeutics).

Highlights

  • The occurrence of cancer is interrelated with human genes

  • Ferroptosis is an important form of regulatory cell death (RCD), caused by the accumulation of lipid free radicals dependent on iron ions, and is lucubrated more extensively in the mechanism of cancer treatment [3]

  • SLC7A11 is upregulated in oral squamous cell carcinoma (OTSCC), excessive intracellular reactive oxygen species (ROS) accumulation, increased O2 concentration, and inhibition of SLC7A11 expression, leading to postirradiation induced ferroptosis, a nanomedicine formed by the combination of the photosensitive agent Ce6 and thickening inducer erastin, and produces good antitumor effects in transplanted tumor mouse models with low other tissue cytotoxicity [105]

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Summary

Introduction

The occurrence of cancer is interrelated with human genes. Mainstream tumor therapy includes surgery, gene therapy (targeted therapy), and immune-related therapy. Nanotechnology has the advantages of strong targeting, low system toxicity, controllable drug release performance, and synergistic effects of novel emerging compound therapies and development of targeting research. It can improve the solubility of drugs, prolong plasma half-life, and promote cell internalization and enhancement accumulation at the tumor site, Oxidative Medicine and Cellular Longevity thereby providing some possibilities to eradicate drugresistant cancer cells [13]. We expound on the mechanism and outline the epigenetic effects of ferroptosis and further optimize the treatment of drug-resistant cancer by combining emerging medical technologies with traditional therapies

Mechanism of Ferroptosis
Tumor Therapy Based on Nonepigenetic and Epigenetic of Ferroptosis
Summary and Conclusions
Conflicts of Interest
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