Interplay between ROS and autophagy in cancer cells, from tumor initiation to cancer therapy

Redox Biol. 2015:4:184-92. doi: 10.1016/j.redox.2014.12.003. Epub 2014 Dec 10.

Abstract

Cancer formation is a complex and highly regulated multi-step process which is highly dependent of its environment, from the tissue to the patient. This complexity implies the development of specific treatments adapted to each type of tumor. The initial step of cancer formation requires the transformation of a healthy cell to a cancer cell, a process regulated by multiple intracellular and extracellular stimuli. The further steps, from the anarchic proliferation of cancer cells to form a primary tumor to the migration of cancer cells to distant organs to form metastasis, are also highly dependent of the tumor environment but of intracellular molecules and pathways as well. In this review, we will focus on the regulatory role of reactive oxygen species (ROS) and autophagy levels during the course of cancer development, from cellular transformation to the formation of metastasis. These data will allow us to discuss the potential of this molecule or pathway as putative future therapeutic targets.

Keywords: Antioxidant; Autophagy; Cancer; Mitochondria; Mitophagy; ROS.

Publication types

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

MeSH terms

  • AMP-Activated Protein Kinases / genetics
  • AMP-Activated Protein Kinases / metabolism
  • Antineoplastic Agents / therapeutic use
  • Apoptosis Regulatory Proteins / genetics
  • Apoptosis Regulatory Proteins / metabolism
  • Autophagy / genetics*
  • Autophagy-Related Protein-1 Homolog
  • Autophagy-Related Proteins
  • Beclin-1
  • Cell Transformation, Neoplastic / genetics
  • Cell Transformation, Neoplastic / metabolism*
  • Cell Transformation, Neoplastic / pathology
  • Cysteine Endopeptidases / genetics
  • Cysteine Endopeptidases / metabolism
  • Gene Expression Regulation, Neoplastic*
  • Humans
  • Intracellular Signaling Peptides and Proteins / genetics
  • Intracellular Signaling Peptides and Proteins / metabolism
  • Kelch-Like ECH-Associated Protein 1
  • Lymphatic Metastasis
  • Membrane Proteins / genetics
  • Membrane Proteins / metabolism
  • Mitochondria / metabolism
  • Mitochondria / pathology
  • Mitophagy / genetics
  • Neoplasms / drug therapy
  • Neoplasms / genetics
  • Neoplasms / metabolism*
  • Neoplasms / pathology
  • Protein Serine-Threonine Kinases / genetics
  • Protein Serine-Threonine Kinases / metabolism
  • Reactive Oxygen Species / metabolism*
  • Signal Transduction
  • Tumor Microenvironment

Substances

  • Antineoplastic Agents
  • Apoptosis Regulatory Proteins
  • Autophagy-Related Proteins
  • BECN1 protein, human
  • Beclin-1
  • Intracellular Signaling Peptides and Proteins
  • KEAP1 protein, human
  • Kelch-Like ECH-Associated Protein 1
  • Membrane Proteins
  • Reactive Oxygen Species
  • Autophagy-Related Protein-1 Homolog
  • Protein Serine-Threonine Kinases
  • ULK1 protein, human
  • AMP-Activated Protein Kinases
  • ATG4A protein, human
  • Cysteine Endopeptidases