Ezh2 competes with p53 to license lncRNA Neat1 transcription for inflammasome activation

Jia, Yuan; Zhu, Qingchen; Zhang, Xingli; Wen, Zhenzhen; Zhang, Guiheng; Li, Ni; Pei, Yanbo; Wang, Yan; Pei, Siyu; Xu, Jing; Jia, Pan; Peng, Chao; Lu, Wei; Qin, Jun; Cao, Qian; Xiao, Yichuan

doi:10.1038/s41418-022-00992-3

Cited by 17 publications

(15 citation statements)

References 56 publications

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“…There is also recent data that radiation induces p53 in BNL CL2 cells 27 and that NEAT1 is a direct target of p53. 28 , 29 , 30 However, we detected a decrease in NEAT1 in response to radiation. After radiation, the change of molecules is a dynamic process, changing with time, and the change rules are also closely related to the radiation dose.…”

Section: Discussionmentioning

confidence: 53%

Activation of long-non-coding RNA NEAT1 sponging microRNA-147 inhibits radiation damage by targeting PDPK1 in troxerutin radioprotection

Hu¹,

Song²,

Zhang³

et al. 2023

iScience

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Section: Discussionmentioning

confidence: 53%

Activation of long-non-coding RNA NEAT1 sponging microRNA-147 inhibits radiation damage by targeting PDPK1 in troxerutin radioprotection

Hu¹,

Song²,

Zhang³

et al. 2023

iScience

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“…As a major gene involved in tumorigenesis as well as in cancer progression, TP53 regulates distinct structures at the level of nuclear envelope [ 120 ], N6-methyladenosine methylation profile [ 121 ], reticulons [ 122 , 123 ] and distinct nodes of the tumorigenic network [ 124 – 128 ]. Accordingly, very recent advances on the p53 biology [ 129 – 131 ] indicated a significant role for p53 in DNA damage response and apoptotic cell death [ 132 , 133 ], ferroptosis [ 134 ], ribosome biogenesis [ 135 ] as well as ncRNA [ 136 – 139 ]. This complex network is clearly highly relevant for individual treatment [ 140 ] to understand the molecular mechanisms at the bases of malignant progression [ 141 , 142 ] and therefore to identify specific cluster of prognostic markers [ 143 – 145 ], hence constituting the scientific bases for precision medicine [ 146 – 148 ].…”

Section: Single-cell Transcriptomics Of Organoidsmentioning

confidence: 99%

Gene expression in organoids: an expanding horizon

2023

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Recent development of human three-dimensional organoid cultures has opened new doors and opportunities ranging from modelling human development in vitro to personalised cancer therapies. These new in vitro systems are opening new horizons to the classic understanding of human development and disease. However, the complexity and heterogeneity of these models requires cutting-edge techniques to capture and trace global changes in gene expression to enable identification of key players and uncover the underlying molecular mechanisms. Rapid development of sequencing approaches made possible global transcriptome analyses and epigenetic profiling. Despite challenges in organoid culture and handling, these techniques are now being adapted to embrace organoids derived from a wide range of human tissues. Here, we review current state-of-the-art multi-omics technologies, such as single-cell transcriptomics and chromatin accessibility assays, employed to study organoids as a model for development and a platform for precision medicine.

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“…Ezh2 is an important epigenetic modifier that modulates histone 3Lys27 (H3K27) methylation (He et al, 2021) and plays an important role in the regulation of immune cell function (Zhang et al, 2018). Yuan et al (2022) found that p53 in microglia/ macrophages could compete with Ezh2 for the same binding region in the long noncoding RNA NEAT1 promoter, thus antagonizing EZH2-induced NEAT1 transcription and inflammasome activation. In contrast, the deletion of Ezh2 strongly promoted the binding of p53 to NEAT1 and the deacetylation of NEAT1 promoter H3K27, thus inhibiting NEAT1 transcription and inflammasome activation, which proved the epigenetic mechanism of regulating inflammasome activation through the Ezh2/p53 competition model in microglia/macrophages after IS (Figure 2d).…”

Section: Ezh2/p53 Competition Modelmentioning

confidence: 99%

Targeting p53 for neuroinflammation: New therapeutic strategies in ischemic stroke

Gao

Liu

et al. 2023

J of Neuroscience Research

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Ischemic stroke (IS) is characterized by high incidence, high recurrence, and high mortality and places a heavy burden on society and families. The pathological mechanisms of IS are complex, among which secondary neurological impairment mediated by neuroinflammation is considered to be the main factor in cerebral ischemic injury.At present, there is still a lack of specific therapies to treat neuroinflammation. The tumor suppressor protein p53 has long been regarded as a key substance in the regulation of the cell cycle and apoptosis in the past. Recently, studies have found that p53 also plays an important role in neuroinflammatory diseases, such as IS. Therefore, p53 may be a crucial target for the regulation of the neuroinflammatory response. Here, we provide a comprehensive review of the potential of targeting p53 in the treatment of neuroinflammation after IS. We describe the function of p53, the major immune cells involved in neuroinflammation, and the role of p53 in inflammatory responses mediated by these cells. Finally, we summarize the therapeutic strategies of targeting p53 in regulating the neuroinflammatory response after IS to provide new directions and ideas for the treatment of ischemic brain injury.

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Ezh2 competes with p53 to license lncRNA Neat1 transcription for inflammasome activation

Cited by 17 publications

References 56 publications

Activation of long-non-coding RNA NEAT1 sponging microRNA-147 inhibits radiation damage by targeting PDPK1 in troxerutin radioprotection

Activation of long-non-coding RNA NEAT1 sponging microRNA-147 inhibits radiation damage by targeting PDPK1 in troxerutin radioprotection

Gene expression in organoids: an expanding horizon

Targeting p53 for neuroinflammation: New therapeutic strategies in ischemic stroke

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