PRDM Proteins: Molecular Mechanisms in Signal Transduction and Transcriptional Regulation

Zazzo, Erika Di; Rosa, Claudio De; Abbondanza, Ciro; Moncharmont, Bruno

doi:10.3390/biology2010107

Cited by 58 publications

(74 citation statements)

References 134 publications

(172 reference statements)

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“…Additionally, mRNA levels of beige cell markers such as CD137 and T-Box1 ( Tbx1 ), and mitochondria markers such as carnitine palmitoyltransferase 1A (Cpt1a) and Cpt2, were also higher, suggesting beneficial effects of Notch depletion [54]. This has been also confirmed in mouse studies, where Notch specific deletion in inguinal WAT induced Ucp1 , cell death-inducing DFFA-like effector A ( Cidea) , Pgc1α and Prdm16 expression [56]. Consistent with these reports, our data predict an inhibitory effect of EPA on Hif1αn and Notch1 genes, which may increase thermogenesis and energy expenditure by increasing levels of Prdm16 , Pgc1α , and Ucp1 as the key regulators of thermogenesis.…”

Section: Discussionmentioning

confidence: 85%

Transcriptomic and microRNA analyses of gene networks regulated by eicosapentaenoic acid in brown adipose tissue of diet-induced obese mice

Pahlavani

Wijayatunga

Kalupahana

et al. 2018

Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biolog

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Brown adipose tissue (BAT) dissipates chemical energy as heat via thermogenesis and protects against obesity by increasing energy expenditure. However, regulation of BAT by dietary factors remains largely unexplored at the mechanistic level. We investigated the effect of eicosapentaenoic acid (EPA) on BAT metabolism. Male C57BL/6J (B6) mice fed either a high-fat diet (HF, 45% kcal fat) or HF diet supplemented with EPA (HF-EPA, 6.75% kcal EPA) were used for 11 weeks. RNA sequencing (RNA-Seq) and microRNA (miRNA) profiling were performed on RNA from BAT using Illumina HiSeq and miSeq respectively. We conducted pathway analyses using ingenuity pathway analysis software (IPA®) and validated some genes and miRNAs using qPCR. We identified 479 genes that were differentially expressed (2-fold change, n=3, p ≤ 0.05) in BAT from HF compared to HF-EPA. Genes negatively correlated with thermogenesis such as hypoxia Inducible factor 1 alpha subunit inhibitor (Hif1αn), was downregulated by EPA. Pathways related to thermogenesis such as peroxisome proliferator-activated receptor (PPAR) were upregulated by EPA while pathways associated with obesity and inflammation such as nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) were downregulated by EPA. MiRNA profiling identified nine and six miRNAs that were upregulated and downregulated by EPA, respectively (log2 fold change > 1.25, n=3, P ≤ 0.05). Key regulatory miRNAs were involved in thermogenesis, such as miR-455–3p and miR-129–5p were validated using qPCR. In conclusion, the depth of transcriptomic and miRNA profiling revealed novel mRNA-miRNA interaction networks in BAT which are involved in thermogenesis which regulated by EPA.

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Section: Discussionmentioning

confidence: 85%

Transcriptomic and microRNA analyses of gene networks regulated by eicosapentaenoic acid in brown adipose tissue of diet-induced obese mice

Pahlavani

Wijayatunga

Kalupahana

et al. 2018

Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biolog

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“…The paired box transcription factor Pax-5, known as a B-cell-specific activator protein, is a key regulator of lineagespecific gene expression and differentiation in B lymphocytes (Fitzsimmons et al 2001). PRDM (PRDI-BF1 and RIZ homology domain containing) proteins have a pivotal role in the transduction of signals that control cell proliferation and differentiation and, consequently, neoplastic transformation (Zazzo et al 2013). An analysis of position -793 (CT) in the 5' flanking region of the TNFα gene revealed a connection between CCAAT binding factors for the T allele.…”

Section: Discussionmentioning

confidence: 99%

Relationship between polymorphism in the tumour necrosis factor-alpha gene and selected indices and cell subpopulations in naturally bovine leukaemia virus-infected and healthy cows

Bojarojć-Nosowicz¹,

Kaczmarczyk²,

Jastrzębska³

2018

Vet. Med. - Czech

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“…2 The PRDM proteins belong to the SET domain protein family characterized PR domains and zinc fingers, and appear to be transcriptional regulators that either exert enzymatic activity on histones or recruit cofactors to modify target gene expression. 3 PRDM family members are dysregulated in many human diseases, especially in hematological malignancies and solid tumors, acting as tumor suppressors or drivers during the oncogenic processes. 4 For example, in a subset of diffuse large B cell lymphoma, PRDM1 promotes cancer progression and is associated with shorter failure-free survival, while PRDM11 inhibits lymphomagenesis.…”

Section: Introductionmentioning

confidence: 99%

Overexpression of PRDM5 promotes acute myeloid leukemia cell proliferation and migration by activating the JNK pathway

Zhou¹,

Chen²,

et al. 2019

Cancer Medicine

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PRDM family proteins are dysregulated in many human diseases, especially hematological malignancies and solid cancers, and share a unique N‐terminal PR domain followed by zinc fingers toward the C terminus. With a high frequency of DNA promoter hypermethylation, PRDM5 is primarily considered as a tumor suppressor in solid tumors. However, little is known about the function of PRDM5 in blood malignancies, especially acute myeloid leukemia (AML). In this study, we showed that high PRDM5 expression levels were independently correlated with poor overall survival in AML patients. PRDM5 overexpression promoted cell proliferation, colony formation, and migration in vitro and enhanced tumorigenesis in an in vivo xenograft model. Furthermore, we found that PRDM5 overexpression promoted cell cycle progression with the decreased level of cell cycle inhibitors such as p16 and p21, and regulated the expression of epithelial‐mesenchymal transition markers ZO‐1 and Vimentin to promote migration. Moreover, we observed that PRDM5 upregulated the Jun N‐terminal kinase (JNK) signaling pathway and downregulated c‐Myc expression. Pharmacological inhibition of JNK by SP600125 partially abrogated PRDM5‐induced cell proliferation and migration. Taken together, our findings demonstrate that PRDM5 functions as an oncogenic driver in AML via JNK pathway, suggesting that PRDM5 is a potential therapeutic target for AML.

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PRDM Proteins: Molecular Mechanisms in Signal Transduction and Transcriptional Regulation

Cited by 58 publications

References 134 publications

Transcriptomic and microRNA analyses of gene networks regulated by eicosapentaenoic acid in brown adipose tissue of diet-induced obese mice

Transcriptomic and microRNA analyses of gene networks regulated by eicosapentaenoic acid in brown adipose tissue of diet-induced obese mice

Relationship between polymorphism in the tumour necrosis factor-alpha gene and selected indices and cell subpopulations in naturally bovine leukaemia virus-infected and healthy cows

Overexpression of PRDM5 promotes acute myeloid leukemia cell proliferation and migration by activating the JNK pathway

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