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J Cancer Res Clin Oncol. 2015 Dec;141(12):2071-7. doi: 10.1007/s00432-015-1916-3. Epub 2015 Jan 21.

The functional role of peroxiredoxin 3 in reactive oxygen species, apoptosis, and chemoresistance of cancer cells.

Li L1, Yu AQ2,3,4.

Author information

1
Department of Obstetrics and Gynecology, Yantai Affiliated Hospital of Binzhou Medical University, 717 Jinbu Street, Muping-district, Yantai, 264100, China. lilq2005@126.com.
2
Institute of Psychology, Chinese Academy of Sciences, Beijing, 100101, China.
3
Graduate School of Chinese Academy of Sciences, Beijing, 100049, China.
4
Canvard College, Beijing Technology and Business University, Beijing, 101118, China.

Abstract

PURPOSE:

The mammalian peroxiredoxin (PRX) family contains six members that provide antioxidant defense in different cell types by removing reactive oxygen species (ROS) through conserved active cysteines. Different from other members, PRX3 is predominantly located in mitochondria, a major apoptosis mediator. The purpose of this review is to summarize the findings on PRX3 concerning its role in ROS removal, apoptosis, and chemoresistance of cancer cells.

METHODS:

The relevant literature from PubMed and Medline databases is reviewed in this article (1994-2014).

RESULTS:

Because of fast growth and relatively low supply of oxygen in cancer cells, ROS production from mitochondria is exaggerated to an extent that overwhelms cellular antioxidant defenses resulting in oxidative stress. As an active responder to oxidative stress, PRX3 is accordingly up-regulated in cancer cells to remove cellular ROS and inhibit apoptosis, which provides a favorable microenvironment for cell proliferation.

CONCLUSION:

Since most of chemotherapy or radiotherapy for cancers is through ROS increase and apoptotic induction, PRX3 might be involved in the chemotherapeutic resistance of cancers.

KEYWORDS:

Apoptosis; Cancer; Oxidative stress; Peroxiredoxin (PRX); Reactive oxygen species (ROS)

PMID:
25875582
DOI:
10.1007/s00432-015-1916-3
[Indexed for MEDLINE]

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