Structure, function and regulation of jade family PHD finger 1 (JADE1)

Panchenko, Mikhail P.

doi:10.1016/j.gene.2016.05.002

Cited by 23 publications

(20 citation statements)

References 64 publications

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“…PHF17), a transcription factor, contains two variants: JADE1-L (a long form with 842 amino acids) and JADE1-S (a short form without a C-terminal fragment of 333 amino acids) (Borgal et al, 2014 ; Siriwardana et al, 2015 ). Although the role of JADE1 remains elusive, the protein exhibits histone acetyltransferase (HAT) activity and acts as a co-factor of the HBO1 complex in histone H4 acetylation during gene regulation, which plays crucial roles in cell cycle regulation (Panchenko et al, 2004 ; Foy et al, 2008 ; Panchenko, 2016 ; Han et al, 2018 ). The suppression of JADE1 (both JADE1-L and JADE1-S) by siRNA knockdown results in suppression of DNA synthesis in cultured epithelial cell lines and primary fibroblasts (Havasi et al, 2013 ).…”

Section: Discussionmentioning

confidence: 99%

Excessive All-Trans Retinoic Acid Inhibits Cell Proliferation Through Upregulated MicroRNA-4680-3p in Cultured Human Palate Cells

Yoshioka

Ramakrishnan

Shim

et al. 2021

Front. Cell Dev. Biol.

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Cleft palate is the second most common congenital birth defect, and both environmental and genetic factors are involved in the etiology of the disease. However, it remains largely unknown how environmental factors affect palate development. Our previous studies show that several microRNAs (miRs) suppress the expression of genes involved in cleft palate. Here we show that miR-4680-3p plays a crucial role in cleft palate pathogenesis. We found that all-trans retinoic acid (atRA) specifically induces miR-4680-3p in cultured human embryonic palatal mesenchymal (HEPM) cells. Overexpression of miR-4680-3p inhibited cell proliferation in a dose-dependent manner through the suppression of expression of ERBB2 and JADE1, which are known cleft palate-related genes. Importantly, a miR-4680-3p-specific inhibitor normalized cell proliferation and altered expression of ERBB2 and JADE1 in cells treated with atRA. Taken together, our results suggest that upregulation of miR-4680-3p induced by atRA may cause cleft palate through suppression of ERBB2 and JADE1. Thus, miRs may be potential targets for the prevention and diagnosis of cleft palate.

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Section: Discussionmentioning

confidence: 99%

Excessive All-Trans Retinoic Acid Inhibits Cell Proliferation Through Upregulated MicroRNA-4680-3p in Cultured Human Palate Cells

Yoshioka

Ramakrishnan

Shim

et al. 2021

Front. Cell Dev. Biol.

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“… Xu et al (2019) showed that miR-6840-3p bound to ZEB2-AS1 and then targeted PLXNB1 to promote the progression of laryngeal squamous cell carcinoma. JADE2 (gene for apoptosis and differentiation in epithelia 2) is a member of the small JADE family ( Panchenko, 2016 ). Several studies found that JADE2 was associated with histone modification in ovarian cancer and acquired immune deficiency syndrome ( Quintela et al, 2019 ; Maxwell et al, 2020 ).…”

Section: Discussionmentioning

confidence: 99%

Identification of a Potential miRNA–mRNA Regulatory Network Associated With the Prognosis of HBV-ACLF

Xie

Zhang

et al. 2021

Front. Mol. Biosci.

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BackgroundHepatitis B virus-related acute-on-chronic liver failure (HBV-ACLF) is a life-threatening disease with a high mortality rate; the systemic inflammatory response plays a vital role in disease progression. We aimed to determine if a miRNA–mRNA co-regulatory network exists in the peripheral blood mononuclear cells (PBMCs) of HBV-ACLF patients, which might be important for prognosis.MethodsIn patients with HBV-ACLF meeting COSSH-ACLF criteria, age, liver cirrhosis and INR were independent risk factors for 28-day and 90-day poor prognosis. COSSH-ACLFs was a superior prognostic model. mir-6840-3p-JADE2 may promote the progression of ACLF and lead to poor prognosis. Meanwhile, mir-6840-3p and mir-6861-3p can be used as markers of short-term poor prognosis. Finally, ALSS treatment is not only the blood material exchange of patients, but also changes part of the immune state of patients. Among them, cytokine cytokine receptor interaction may play an important role in determining the therapeutic effect.MethodsTranscriptome-wide microRNA (miRNA) and mRNA microarrays were used to define the miRNA and mRNA expression profiles of the PBMCs of HBV-ACLF patients in a discovery cohort. The targets of the miRNAs were predicted. We built a miRNA-mRNA regulatory network through bioinformatics analysis, and used quantitative real-time polymerase chain reaction (qRT-PCR) to assess the importance of candidate miRNAs and mRNAs. We also assessed the direct and transcriptional regulatory effects of miRNAs on target mRNAs using a dual-luciferase reporter assay.ResultsThe miRNA/mRNA PBMC expression profiles of the discovery cohort, of whom eight survived and eight died, revealed a prognostic interactive network involving 38 miRNAs and 313 mRNAs; this was constructed by identifying the target genes of the miRNAs. We validated the expression data in another cohort, of whom 43 survived and 35 died; miR-6840-3p, miR-6861-3p, JADE2, and NR3C2 were of particular interest. The levels of miR-6840-3p and miR-6861-3p were significantly increased in the PBMCs of the patients who died, and thus predicted prognosis (areas under the curve values = 0.665 and 0.700, respectively). The dual-luciferase reporter assay indicated that miR-6840-3p directly targeted JADE2.ConclusionWe identified a prognostic miRNA-mRNA co-regulatory network in the PBMCs of HBV-ACLF patients. miR-6840-3p-JADE2 is a potential miRNA–mRNA pair contributing to a poor prognosis.

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“…[30][31][32] Phf16 is a member of a family of large proteins containing plant homeo domain (PHD)-type zinc fingers. 33 However, functions of Pnpla3 and Phf16 in adipocyte differentiation remain unclear. Therefore, further analyses may provide insights into the roles of Pnpla3 and Phf16 genes in adipocyte differentiation.…”

Section: Discussionmentioning

confidence: 99%

Identification of Phf16 and Pnpla3 as new adipogenic factors regulated by phytochemicals

Chang

Yun

Choi

et al. 2018

J of Cellular Biochemistry

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Adipocyte differentiation is controlled by multiple signaling pathways. To identify new adipogenic factors, C3H10T1/2 adipocytes were treated with previously known antiadipogenic phytochemicals (resveratrol, butein, sulfuretin, and fisetin) for 24 hours. Commonly regulated genes were then identified by transcriptional profiling analysis. Three genes (chemokine (C-X-C motif) ligand 1 [Cxcl1], heme oxygenase 1 [Hmox1], and PHD (plant homeo domain) finger protein 16 [Phf16]) were upregulated while two genes (G0/G1 switch gene 2 [G0s2] and patatin-like phospholipase domain containing 3 [Pnpla3]) were downregulated by these four antiadipogenic compounds. Tissue expression profiles showed that the G0s2 and Pnpla3 expressions were highly specific to adipose depots while the other three induced genes were ubiquitously expressed with significantly higher expression in adipose tissues. While Cxcl1 expression was decreased, expressions of the other four genes were significantly increased during adipogenic differentiation of C3H10T1/2 cells. Small interfering RNA–mediated knockdown including Phf16 and Pnpla3 indicated that these genes might play regulatory roles in lipid accumulation and adipocyte differentiation. Specifically, the silencing of two newly identified adipogenic genes, Phf16 or Pnpla3, suppressed lipid accumulation and expression of adipocyte markers in both 3T3-L1 and C3H10T1/2 cells. Taken together, these data showed previously uncovered roles of Phf16 and Pnpla3 in adipogenesis, highlighting the potential of using phytochemicals for further investigation of adipocyte biology.

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Structure, function and regulation of jade family PHD finger 1 (JADE1)

Cited by 23 publications

References 64 publications

Excessive All-Trans Retinoic Acid Inhibits Cell Proliferation Through Upregulated MicroRNA-4680-3p in Cultured Human Palate Cells

Excessive All-Trans Retinoic Acid Inhibits Cell Proliferation Through Upregulated MicroRNA-4680-3p in Cultured Human Palate Cells

Identification of a Potential miRNA–mRNA Regulatory Network Associated With the Prognosis of HBV-ACLF

Identification of Phf16 and Pnpla3 as new adipogenic factors regulated by phytochemicals

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