Volume 233, Issue 7 p. 5119-5132
MINI-REVIEW

Reactive oxygen species and colorectal cancer

Sisi Lin

Sisi Lin

Department of Pathophysiology, Institute of Digestive Disease, Tongji University School of Medicine, Shanghai, China

Department of General, Visceral, and Transplant Surgery, Ludwig–Maximilians—University Munich, Munich, Germany

Search for more papers by this author
Yongyu Li

Yongyu Li

Department of Pathophysiology, Institute of Digestive Disease, Tongji University School of Medicine, Shanghai, China

Search for more papers by this author
Andrey A. Zamyatnin Jr.

Andrey A. Zamyatnin Jr.

Institute of Molecular Medicine, Sechenov First Moscow State Medical University, Moscow, Russia

Department of Cell Signalling, Belozersky Institute of Physico–Chemical Biology, Lomonosov Moscow State University, Moscow, Russia

Search for more papers by this author
Jens Werner

Jens Werner

Department of General, Visceral, and Transplant Surgery, Ludwig–Maximilians—University Munich, Munich, Germany

German Cancer Consortium (DKTK), Partner Site Munich, Munich, Germany

Search for more papers by this author
Alexandr V. Bazhin

Corresponding Author

Alexandr V. Bazhin

Department of General, Visceral, and Transplant Surgery, Ludwig–Maximilians—University Munich, Munich, Germany

German Cancer Consortium (DKTK), Partner Site Munich, Munich, Germany

Correspondence

Alexandr V. Bazhin, Department of General, Visceral, and Transplant Surgery, Ludwig–Maximilians—University Munich, 81377 Munich, Germany.

Email: [email protected]

Search for more papers by this author
First published: 07 December 2017
Citations: 94

Abstract

Colorectal cancer (CRC) has become the fourth leading cause of cancer-related death in the worldwide. It is urgent to find more effective therapeutic strategies for it. Reactive oxygen species (ROS) play multiple roles in normal cellular physiology processes. Thus, a certain level of ROS is essential to keep normal cellular function. However, the accumulation of ROS shows dual roles for cells, which is mainly dependent on the concentration of ROS, the origin of the cancer cell and the activated signaling pathways during tumor progression. In general, moderate level of ROS leads to cell damage, DNA mutation and inflammation, which promotes the initiation and development of cancer. Excessive high level of ROS induces cancer cell death, showing an anti-cancer role. ROS are commonly higher in CRC cells than their normal counterpart cells. Therefore, it is possible that ROS induce cell death in cancer cells while not affecting the normal cells, demonstrating lower side effects. Besides, ROS also play a role in tumor microenvironment and drug resistance. These multiple roles of ROS make them a promising therapeutic target for cancer. To explore potential ROS-target therapies against CRC, it is worth to comprehensively understanding the role of ROS in CRC and therapy. In this review, we mainly discuss the strategies of ROS in CRC therapy, including direct CRC cell target and indirect tumor environment target. In addition, the influences of ROS in drug resistance will also been discussed.

CONFLICTS OF INTEREST

The authors declare no conflicts of interest.

The full text of this article hosted at iucr.org is unavailable due to technical difficulties.