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Redox Regulation of PTEN by Peroxiredoxins

Title
Redox Regulation of PTEN by Peroxiredoxins
Authors
Nguyen Huu, ThangPark, JiyoungZhang, YingPark, IhaYoon, Hyun JoongWoo, Hyun AeLee, Seung-Rock
Ewha Authors
우현애
SCOPUS Author ID
우현애scopus
Issue Date
2021
Journal Title
ANTIOXIDANTS
ISSN
2076-3921JCR Link
Citation
ANTIOXIDANTS vol. 10, no. 2
Keywords
PTENredox regulationperoxiredoxins
Publisher
MDPI
Indexed
SCIE; SCOPUS WOS scopus
Document Type
Review
Abstract
Phosphatase and tensin homolog deleted on chromosome 10 (PTEN) is known as a tumor suppressor gene that is frequently mutated in numerous human cancers and inherited syndromes. PTEN functions as a negative regulator of PI3K/Akt signaling pathway by dephosphorylating phosphatidylinositol (3, 4, 5)-trisphosphate (PIP3) to phosphatidylinositol (4, 5)-bisphosphate (PIP2), which leads to the inhibition of cell growth, proliferation, cell survival, and protein synthesis. PTEN contains a cysteine residue in the active site that can be oxidized by peroxides, forming an intramolecular disulfide bond between Cys(124) and Cys(71). Redox regulation of PTEN by reactive oxygen species (ROS) plays a crucial role in cellular signaling. Peroxiredoxins (Prxs) are a superfamily of peroxidase that catalyzes reduction of peroxides and maintains redox homeostasis. Mammalian Prxs have 6 isoforms (I-VI) and can scavenge cellular peroxides. It has been demonstrated that Prx I can preserve and promote the tumor-suppressive function of PTEN by preventing oxidation of PTEN under benign oxidative stress via direct interaction. Also, Prx II-deficient cells increased PTEN oxidation and insulin sensitivity. Furthermore, Prx III has been shown to protect PTEN from oxidation induced by 15s-HpETE and 12s-HpETE, these are potent inflammatory and pro-oxidant mediators. Understanding the tight connection between PTEN and Prxs is important for providing novel therapies. Herein, we summarized recent studies focusing on the relationship of Prxs and the redox regulation of PTEN.
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DOI
10.3390/antiox10020302
Appears in Collections:
약학대학 > 약학과 > Journal papers
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