Redox Regulation of PTEN by Peroxiredoxins

Huu, Thang Nguyen; Park, Jiyoung; Zhang, Ying; Park, Iha; Yoon, Hyun Joong; Woo, Hyun Ae; Lee, Seung Rock

doi:10.3390/antiox10020302

Cited by 26 publications

(17 citation statements)

References 113 publications

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“…Some members of the Prx family (Prx1-5) act as downstream signaling mediators for several key signaling pathways controlled by MAP3Ks, such as apoptosis signalregulating kinase 1 [190], MEKK4 [191], and PTEN [192]. Prxs are unique compared to other antioxidant enzymes due to their high reactivity with H 2 O 2 , which itself does not always oxidize downstream targets, because of its relatively low physiological concentrations (< 100 nM) in muscle cells, even after an exercise stimulus [189].…”

Section: Peroxiredoxins and Redox Signalingmentioning

confidence: 99%

Redox Signaling and Sarcopenia: Searching for the Primary Suspect

Foreman

Hesse

2021

IJMS

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Sarcopenia, the age-related decline in muscle mass and function, derives from multiple etiological mechanisms. Accumulative research suggests that reactive oxygen species (ROS) generation plays a critical role in the development of this pathophysiological disorder. In this communication, we review the various signaling pathways that control muscle metabolic and functional integrity such as protein turnover, cell death and regeneration, inflammation, organismic damage, and metabolic functions. Although no single pathway can be identified as the most crucial factor that causes sarcopenia, age-associated dysregulation of redox signaling appears to underlie many deteriorations at physiological, subcellular, and molecular levels. Furthermore, discord of mitochondrial homeostasis with aging affects most observed problems and requires our attention. The search for the primary suspect of the fundamental mechanism for sarcopenia will likely take more intense research for the secret of this health hazard to the elderly to be unlocked.

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Section: Peroxiredoxins and Redox Signalingmentioning

confidence: 99%

Redox Signaling and Sarcopenia: Searching for the Primary Suspect

Foreman

Hesse

2021

IJMS

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“…In addition, recent reports have revealed that SIPL1 activates the AKT pathway by directly binding to and inactivating PTEN in human cancer cells both in vitro and in vivo (24). Loss of PTEN is the primary mechanism that activates the PI3K/AKT pathway in mice and cells (35,36).…”

Section: Discussionmentioning

confidence: 99%

SIPL1, Regulated by MAZ, Promotes Tumor Progression and Predicts Poor Survival in Human Triple-Negative Breast Cancer

He¹,

Wang²,

Teng³

et al. 2021

Front. Oncol.

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BackgroundTriple-negative breast cancer (TNBC) is an aggressive subtype of breast cancer owing to a lack of effective targeted therapy and acquired chemoresistance. Here, we explored the function and mechanism of shank-interacting protein-like 1 (SIPL1) in TNBC progression.MethodsSIPL1 expression was examined in human TNBC tissues and cell lines by quantitative reverse transcription PCR, western blot, and immunohistochemistry. SIPL1 overexpression and silenced cell lines were established in BT-549 and MDA-MB-231 cells. The biological functions of SIPL1 in TNBC were studied in vitro using the CCK-8 assay, CellTiter-Glo Luminescent Cell Viability assay, caspase-3/8/9 assay, wound healing assay, and transwell assay and in vivo using a nude mouse model. The potential mechanisms underlying the effects of SIPL1 on TNBC progression were explored using bioinformatics analysis, luciferase reporter assays, and chromatin immunoprecipitation followed by qPCR.ResultsSIPL1 expression was higher in human TNBC tissues and cell lines than in adjacent normal tissues and a breast epithelial cell line (MCF10A). High expression of SIPL1 was positively correlated with poor overall and disease-free survival in patients with TNBC. SIPL1 overexpression elevated and SIPL1 silencing repressed the malignant phenotypes of TNBC cells in vitro. SIPL1 overexpression promoted xenograft tumor growth in vivo. Myc-associated zinc-finger protein (MAZ) transcriptionally activated SIPL1. Finally, we found that SIPL1 promoted TNBC malignant phenotypes via activation of the AKT/NF-κB signaling pathways.ConclusionsThese results indicate that the MAZ/SIPL1/AKT/NF-κB axis plays a crucial role in promoting the malignant phenotypes of TNBC cells.

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“…To prevent inactivation of these phosphatases, several defensive systems are available, and these function to maintain ROS signaling in an appropriate range. As detailed below, peroxiredoxins (PRDXs), which exhibit thioredoxin (TRX)-dependent peroxidase activity, have a regulatory role in restricting hydrogen peroxide levels, thereby maintaining normal ROS signaling [3,29].…”

Section: Nadph Oxidasesmentioning

confidence: 99%

Superoxide Radicals in the Execution of Cell Death

2022

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Superoxide is a primary oxygen radical that is produced when an oxygen molecule receives one electron. Superoxide dismutase (SOD) plays a primary role in the cellular defense against an oxidative insult by ROS. However, the resulting hydrogen peroxide is still reactive and, in the presence of free ferrous iron, may produce hydroxyl radicals and exacerbate diseases. Polyunsaturated fatty acids are the preferred target of hydroxyl radicals. Ferroptosis, a type of necrotic cell death induced by lipid peroxides in the presence of free iron, has attracted considerable interest because of its role in the pathogenesis of many diseases. Radical electrons, namely those released from mitochondrial electron transfer complexes, and those produced by enzymatic reactions, such as lipoxygenases, appear to cause lipid peroxidation. While GPX4 is the most potent anti-ferroptotic enzyme that is known to reduce lipid peroxides to alcohols, other antioxidative enzymes are also indirectly involved in protection against ferroptosis. Moreover, several low molecular weight compounds that include α-tocopherol, ascorbate, and nitric oxide also efficiently neutralize radical electrons, thereby suppressing ferroptosis. The removal of radical electrons in the early stages is of primary importance in protecting against ferroptosis and other diseases that are related to oxidative stress.

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Redox Regulation of PTEN by Peroxiredoxins

Cited by 26 publications

References 113 publications

Redox Signaling and Sarcopenia: Searching for the Primary Suspect

Redox Signaling and Sarcopenia: Searching for the Primary Suspect

SIPL1, Regulated by MAZ, Promotes Tumor Progression and Predicts Poor Survival in Human Triple-Negative Breast Cancer

Superoxide Radicals in the Execution of Cell Death

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