Redox regulation of cancer metastasis: molecular signaling and therapeutic opportunities

Drug Dev Res. 2014 Aug;75(5):331-41. doi: 10.1002/ddr.21216.

Abstract

Cancer metastasis is the major cause of cancer-related mortality. Accumulated evidence has shown that high-metastasis potential cancer cells have more reactive oxygen species (ROS) accumulation compared with low-metastasis potential cancer cells. ROS can function as second messengers to regulate multiple cancer metastasis-related signaling pathways via reversible oxidative posttranslational modifications of cysteine in key redox-sensitive proteins, which leads to the structural and functional change of these proteins. Because ROS can promote cancer metastasis, therapeutic strategies aiming at inducing/reducing cellular ROS level or targeting redox sensors involved in metastasis hold great potential in developing new efficient approaches for anticancer therapy. In this review, we summarize recent findings on regulation of tumor metastasis by key redox sensors and describe the potential of targeting redox signaling pathways for cancer therapy.

Keywords: cancer therapy; metastasis; reactive oxygen species; redox sensors.

Publication types

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

MeSH terms

  • Antineoplastic Agents / therapeutic use
  • Combined Modality Therapy
  • Humans
  • Neoplasm Metastasis / drug therapy*
  • Neoplasm Metastasis / radiotherapy
  • Neoplasms / drug therapy
  • Neoplasms / metabolism
  • Neoplasms / radiotherapy
  • Oxidation-Reduction
  • Oxidative Stress
  • Reactive Oxygen Species / metabolism*
  • Signal Transduction

Substances

  • Antineoplastic Agents
  • Reactive Oxygen Species