The epigenetic regulators and metabolic changes in ferroptosis-associated cancer progression

Mol Cancer. 2020 Feb 27;19(1):39. doi: 10.1186/s12943-020-01157-x.

Abstract

Ferroptosis, a novel form of regulated cell death, is different from other types of cell death in morphology, genetics and biochemistry. Increasing evidence indicates that ferroptosis has significant implications on cell death linked to cardiomyopathy, tumorigenesis, and cerebral hemorrhage to name a few. Here we summarize current literature on ferroptosis, including organelle dysfunction, signaling transduction pathways, metabolic reprogramming and epigenetic regulators in cancer progression. With regard to organelles, mitochondria-induced cysteine starvation, endoplasmic reticulum-related oxidative stress, lysosome dysfunction and golgi stress-related lipid peroxidation all contribute to induction of ferroptosis. Understanding the underlying mechanism in ferroptosis could provide insight into the treatment of various intractable diseases including cancers.

Keywords: Cancer; Chromatin remodeling factor; Endoplasmic reticulum; Epigenetics; Ferroptosis; Golgi; Immunotherapy; Iron; Lipid peroxidation; Lysosome; Metabolism; Mitochondria; Organelles; lncRNA.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Biological Transport
  • Endoplasmic Reticulum Stress*
  • Epigenesis, Genetic*
  • Ferroptosis*
  • Humans
  • Mitochondria / genetics
  • Mitochondria / metabolism
  • Mitochondria / pathology*
  • Neoplasms / genetics
  • Neoplasms / pathology*
  • Reactive Oxygen Species
  • Signal Transduction

Substances

  • Reactive Oxygen Species