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Novel roles of peroxiredoxins in inflammation, cancer and innate immunity.

Ishii T, Warabi E, Yanagawa T - J Clin Biochem Nutr (2012)

Bottom Line: Extracellular peroxiredoxin 1 and peroxiredoxin 2 are known to enhance natural killer cell activity and suppress virus-replication in cells.Peroxiredoxin 1-deficient mice show reduced antioxidant activities but also exhibit restrained tissue inflammatory reactions under some patho-physiological conditions.Novel functions of peroxiredoxins in inflammation, cancer and innate immunity are the focus of this review.

View Article: PubMed Central - PubMed

Affiliation: Majors of Medical Sciences, Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Ibaraki 305-8575, Japan.

ABSTRACT
Peroxiredoxins possess thioredoxin or glutathione peroxidase and chaperone-like activities and thereby protect cells from oxidative insults. Recent studies, however, reveal additional functions of peroxiredoxins in gene expression and inflammation-related biological reactions such as tissue repair, parasite infection and tumor progression. Notably, peroxiredoxin 1, the major mammalian peroxiredoxin family protein, directly interacts with transcription factors such as c-Myc and NF-κB in the nucleus. Additionally, peroxiredoxin 1 is secreted from some cells following stimulation with TGF-β and other cytokines and is thus present in plasma and body fluids. Peroxiredoxin 1 is now recognized as one of the pro-inflammatory factors interacting with toll-like receptor 4, which triggers NF-κB activation and other signaling pathways to evoke inflammatory reactions. Some cancer cells release peroxiredoxin 1 to stimulate toll-like receptor 4-mediated signaling for their progression. Interestingly, peroxiredoxins expressed in protozoa and helminth may modulate host immune responses partly through toll-like receptor 4 for their survival and progression in host. Extracellular peroxiredoxin 1 and peroxiredoxin 2 are known to enhance natural killer cell activity and suppress virus-replication in cells. Peroxiredoxin 1-deficient mice show reduced antioxidant activities but also exhibit restrained tissue inflammatory reactions under some patho-physiological conditions. Novel functions of peroxiredoxins in inflammation, cancer and innate immunity are the focus of this review.

No MeSH data available.


Related in: MedlinePlus

Roles of nuclear Prx1 and Prx2. Prx1 is localized in both the cytoplasm and nucleus and interacts directly with the transcription factors, c-Myc,(56) NF-κB(22,59) and AR.(24) Prx1 suppress c-Myc,(23,56) whereas it enhances activities of p50(22) and p65(59) components of NF-κB and helps activation/phosphorylation of AR.(24) Prx2 is also localized in the nucleus and enhances JNK signaling induced by anticancer/DNA-damaging agent resulting in DNA-repair and tumor survival.(53) Cytoplasmic Prx2 increases AR transactivation, whereas nuclear Prx2 suppresses AR transactivation.
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Figure 2: Roles of nuclear Prx1 and Prx2. Prx1 is localized in both the cytoplasm and nucleus and interacts directly with the transcription factors, c-Myc,(56) NF-κB(22,59) and AR.(24) Prx1 suppress c-Myc,(23,56) whereas it enhances activities of p50(22) and p65(59) components of NF-κB and helps activation/phosphorylation of AR.(24) Prx2 is also localized in the nucleus and enhances JNK signaling induced by anticancer/DNA-damaging agent resulting in DNA-repair and tumor survival.(53) Cytoplasmic Prx2 increases AR transactivation, whereas nuclear Prx2 suppresses AR transactivation.

Mentions: Prx1 is localized in the nucleus as well as in the cytoplasm and has been shown to interact with transcription factors such as c-Myc, NF-κB and AR to modulate their activities (Fig. 2). The effects of nuclear Prx1 on gene expression via c-Myc are especially important for elucidating the phenotype of Prx1-deficient mice as will be discussed in later sections. Prx2 also localizes in both the nucleus and cytoplasm to protect cancer cells from chemotherapeutic agents.(51)


Novel roles of peroxiredoxins in inflammation, cancer and innate immunity.

Ishii T, Warabi E, Yanagawa T - J Clin Biochem Nutr (2012)

Roles of nuclear Prx1 and Prx2. Prx1 is localized in both the cytoplasm and nucleus and interacts directly with the transcription factors, c-Myc,(56) NF-κB(22,59) and AR.(24) Prx1 suppress c-Myc,(23,56) whereas it enhances activities of p50(22) and p65(59) components of NF-κB and helps activation/phosphorylation of AR.(24) Prx2 is also localized in the nucleus and enhances JNK signaling induced by anticancer/DNA-damaging agent resulting in DNA-repair and tumor survival.(53) Cytoplasmic Prx2 increases AR transactivation, whereas nuclear Prx2 suppresses AR transactivation.
© Copyright Policy - open-access
Related In: Results  -  Collection

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Figure 2: Roles of nuclear Prx1 and Prx2. Prx1 is localized in both the cytoplasm and nucleus and interacts directly with the transcription factors, c-Myc,(56) NF-κB(22,59) and AR.(24) Prx1 suppress c-Myc,(23,56) whereas it enhances activities of p50(22) and p65(59) components of NF-κB and helps activation/phosphorylation of AR.(24) Prx2 is also localized in the nucleus and enhances JNK signaling induced by anticancer/DNA-damaging agent resulting in DNA-repair and tumor survival.(53) Cytoplasmic Prx2 increases AR transactivation, whereas nuclear Prx2 suppresses AR transactivation.
Mentions: Prx1 is localized in the nucleus as well as in the cytoplasm and has been shown to interact with transcription factors such as c-Myc, NF-κB and AR to modulate their activities (Fig. 2). The effects of nuclear Prx1 on gene expression via c-Myc are especially important for elucidating the phenotype of Prx1-deficient mice as will be discussed in later sections. Prx2 also localizes in both the nucleus and cytoplasm to protect cancer cells from chemotherapeutic agents.(51)

Bottom Line: Extracellular peroxiredoxin 1 and peroxiredoxin 2 are known to enhance natural killer cell activity and suppress virus-replication in cells.Peroxiredoxin 1-deficient mice show reduced antioxidant activities but also exhibit restrained tissue inflammatory reactions under some patho-physiological conditions.Novel functions of peroxiredoxins in inflammation, cancer and innate immunity are the focus of this review.

View Article: PubMed Central - PubMed

Affiliation: Majors of Medical Sciences, Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Ibaraki 305-8575, Japan.

ABSTRACT
Peroxiredoxins possess thioredoxin or glutathione peroxidase and chaperone-like activities and thereby protect cells from oxidative insults. Recent studies, however, reveal additional functions of peroxiredoxins in gene expression and inflammation-related biological reactions such as tissue repair, parasite infection and tumor progression. Notably, peroxiredoxin 1, the major mammalian peroxiredoxin family protein, directly interacts with transcription factors such as c-Myc and NF-κB in the nucleus. Additionally, peroxiredoxin 1 is secreted from some cells following stimulation with TGF-β and other cytokines and is thus present in plasma and body fluids. Peroxiredoxin 1 is now recognized as one of the pro-inflammatory factors interacting with toll-like receptor 4, which triggers NF-κB activation and other signaling pathways to evoke inflammatory reactions. Some cancer cells release peroxiredoxin 1 to stimulate toll-like receptor 4-mediated signaling for their progression. Interestingly, peroxiredoxins expressed in protozoa and helminth may modulate host immune responses partly through toll-like receptor 4 for their survival and progression in host. Extracellular peroxiredoxin 1 and peroxiredoxin 2 are known to enhance natural killer cell activity and suppress virus-replication in cells. Peroxiredoxin 1-deficient mice show reduced antioxidant activities but also exhibit restrained tissue inflammatory reactions under some patho-physiological conditions. Novel functions of peroxiredoxins in inflammation, cancer and innate immunity are the focus of this review.

No MeSH data available.


Related in: MedlinePlus