Genotoxic stress-triggered β-catenin/JDP2/PRMT5 complex facilitates reestablishing glutathione homeostasis

Cao, Lixue; Wu, Geyan; Zhu, Jinrong; Tan, Zhanyao; Shi, Dongni; Wu, Xingui; Tang, Miaoling; Li, Ziwen; Hu, Yameng; Zhang, Shuxia; Yu, Ruyuan; Mo, Shuang; Wu, Jueheng; Song, Erwei; Li, Mengfeng; Song, Libing; Li, Jun

doi:10.1038/s41467-019-11696-7

Cited by 39 publications

(27 citation statements)

References 49 publications

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“…Alterations in the ratio of the redox pair 2GSH/GSSG towards a more oxidized status form the biochemical basis of targeting redox-sensitive cysteine residues in proteins. As an antioxidant, GSH removes ROS directly or indirectly and limits the lifetime of the oxidative signal [33]. GSH is also a substrate of several antioxidant enzymes.…”

Section: Ros and Antioxidant Pathwaysmentioning

confidence: 99%

Reactive Oxygen Species as a Link between Antioxidant Pathways and Autophagy

Ding

et al. 2021

Oxidative Medicine and Cellular Longevity

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Reactive oxygen species (ROS) are highly reactive molecules that can oxidize proteins, lipids, and DNA. Under physiological conditions, ROS are mainly generated in the mitochondria during aerobic metabolism. Under pathological conditions, excessive ROS disrupt cellular homeostasis. High levels of ROS result in severe oxidative damage to the cellular machinery. However, a low/mild level of ROS could serve as a signal to trigger cell survival mechanisms. To prevent and cope with oxidative damage to biomolecules, cells have developed various antioxidant and detoxifying mechanisms. Meanwhile, ROS can initiate autophagy, a process of self-clearance, which helps to reduce oxidative damage by engulfing and degrading oxidized substance. This review summarizes the interactions among ROS, autophagy, and antioxidant pathways. The effects of natural phytochemicals on autophagy induction, antioxidation, and dual-function are also discussed.

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Section: Ros and Antioxidant Pathwaysmentioning

confidence: 99%

Reactive Oxygen Species as a Link between Antioxidant Pathways and Autophagy

Ding

et al. 2021

Oxidative Medicine and Cellular Longevity

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“…Histone methylation is found among basic amino acid lysine, arginine and histidine [121]. Numerous studies have demonstrated the significant role of histone methylation in breast cancer progression and metastasis [122,123]. [112,114] 5.…”

Section: Histone Modifications and Their Role Is Breast Cancer Metastmentioning

confidence: 99%

A three layered histone epigenetics in breast cancer metastasis

2020

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Thanks to the advancement in science and technology and a significant number of cancer research programs being carried out throughout the world, the prevention, prognosis and treatment of breast cancer are improving with a positive and steady pace. However, a stern thoughtful attention is required for the metastatic breast cancer casesthe deadliest of all types of breast cancer, with a character of relapse even when treated. In an effort to explore the less travelled avenues, we summarize here studies underlying the aspects of histone epigenetics in breast cancer metastasis. Authoritative reviews on breast cancer epigenetics are already available; however, there is an urgent need to focus on the epigenetics involved in metastatic character of this cancer. Here we put forward a comprehensive review on how different layers of histone epigenetics comprising of histone chaperones, histone variants and histone modifications interplay to create breast cancer metastasis landscape. Finally, we propose a hypothesis of integrating histone-epigenetic factors as biomarkers that encompass different breast cancer subtypes and hence could be exploited as a target of larger population.

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“…Genotoxic stress, including chemotherapy, induces interaction between β-catenin, ATM-phosphorylated JDP2 (Jun dimerization protein 2) and PRMT5, resulting in transcription of genes implicated in redox homeostasis. In this process, H3R2me1/H3R2me2s catalyzed by PRMT5 recruits the WDR5/MLL complex resulting in H3K4me3 and transcriptional activation of redox-related genes [39]. PRMT5 forms a complex with the adaptor protein SHARPIN implicated in H3R2me1 modification and recruitment of WDR5-ASH2 (MLL-component), facilitating formation of H3K4me3 on genes functioning in metastasis [40].…”

Section: Prmt5 Control Of Gene Expression By Histone Methylationmentioning

confidence: 99%

PRMT5 function and targeting in cancer

Kim¹,

Ronai²

2020

CST

152

131

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Protein methyl transferases play critical roles in numerous regulatory pathways that underlie cancer development, progression and therapyresponse. Here we discuss the function of PRMT5, a member of the nine-member PRMT family, in controlling oncogenic processes including tumor intrinsic, as well as extrinsic microenvironmental signaling pathways. We discuss PRMT5 effect on histone methylation and methylation of regulatory proteins including those involved in RNA splicing, cell cycle, cell death and metabolic signaling. In all, we highlight the importance of PRMT5 regulation and function in cancer, which provide the foundation for therapeutic modalities targeting PRMT5.

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Genotoxic stress-triggered β-catenin/JDP2/PRMT5 complex facilitates reestablishing glutathione homeostasis

Cited by 39 publications

References 49 publications

Reactive Oxygen Species as a Link between Antioxidant Pathways and Autophagy

Reactive Oxygen Species as a Link between Antioxidant Pathways and Autophagy

A three layered histone epigenetics in breast cancer metastasis

PRMT5 function and targeting in cancer

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