Set7 mediated interactions regulate transcriptional networks in embryonic stem cells

Tuano, Natasha; Okabe, Jun; Ziemann, Mark; Cooper, Mark E.; El‐Osta, Assam

doi:10.1093/nar/gkw621

Cited by 17 publications

(33 citation statements)

References 53 publications

(79 reference statements)

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“…Additional evidence further supports SETD7 involvement in hESCs differentiation, as SETD7 knockdown impedes silencing of pluripotent markers and delays differentiation 49 . These findings support that SETD7 is upregulated during cell differentiation 45,47,49,50 . Accordingly, increased Setd7 levels during mESC differentiation mediate Setd7-dependent H3K4me1 to regulate genes associated with differentiation and induce smooth muscle-associated genes 47 .…”

Section: Ezh2supporting

confidence: 80%

“…More recently, a flurry of studies has reported substantial roles for SETD7 involvement in ESC pluripotency both through transcriptionally regulated pathways, and direct methylation of pluripotent substrates, such as SOX2 and LIN28A 45,46 . Oct4 and Sox2 suppress Setd7 expression levels in mESCs by binding to its promoter region, whereas upon differentiation, removal of these pluripotency factors induces Setd7 transcription by activating H3K4me3 marks at bivalent domains 47 . Consistent with these findings, Babaie et al reported upregulation of SETD7 in hESCs after knockdown of OCT4, supporting intricate roles of these factors as it pertains to ESC pluripotency 48 .…”

Section: Ezh2mentioning

confidence: 99%

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Critical roles of protein methyltransferases and demethylases in the regulation of embryonic stem cell fate

2017

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Accumulating evidence has recently shown that protein methyltransferases and demethylases are crucial regulators in either maintaining pluripotent states or inducing differentiation of embryonic stem cells. These enzymes control pluripotent signatures by mediating activation or repression of histone marks, or through direct methylation of non-histone proteins. Importantly, chromatin modifiers can influence the fate of many differentiation-related genes by loosening chromatin and allowing for transcriptional activation of lineage-specific genes. Genome-wide studies have unraveled diverse changes in methylation patterns following embryonic stem cell differentiation, with redistribution of heterochromatic and euchromatic marks, underlying the importance of chromatin modifiers in governing the fate of embryonic stemness. Furthermore, the development of small molecule inhibitors targeting these agents may shed light in potential clinical implementation to reprogram embryonic stem cells for biomedical therapeutics. Ever since the pioneering introduction of induced pluripotent stem cells, the challenge for application in regenerative medicine and broader medical therapeutics has commenced.

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Section: Ezh2supporting

confidence: 80%

Section: Ezh2mentioning

confidence: 99%

Critical roles of protein methyltransferases and demethylases in the regulation of embryonic stem cell fate

2017

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“…The stimulation of transcriptional activation involves numerous diverse classes of proteins known as transcription coactivators 30,31 . SET7/9 catalyzes the monomethylation of histone H3 lysine 4 (H3K4me1) and nonhistone proteins such as serum response factor in embryonic stem cells to regulate gene expression as coactivators 32 . In breast cancer, as reported by Subramanian K. et al 33 , estrogen receptor α (ER) is a liganddependent transcription factor that can be directly methylated by SET7/9.…”

Section: Discussionmentioning

confidence: 99%

SET7/9 promotes multiple malignant processes in breast cancer development via RUNX2 activation and is negatively regulated by TRIM21

Zhou

Zhao

et al. 2020

Cell Death Dis

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Although the deregulation of lysine methyltransferase (su(var)-3-9, enhancer-of-zeste, trithorax) domain-containing protein 7/9 (SET7/9) has been identified in a variety of cancers, the potential role of SET7/9 and the molecular events in which it is involved in breast cancer remain obscure. Using the online Human Protein Atlas and GEO databases, the expression of SET7/9 was analyzed. Furthermore, we investigated the underlying mechanisms using chromatin immunoprecipitation-based deep sequencing (ChIP-seq) and quantitative ChIP assays. To explore the physiological role of SET7/9, functional analyses such as CCK-8, colony formation, and transwell assays were performed and a xenograft tumor model was generated with the human breast cancer cell lines MCF-7 and MDA-MB-231. Mass spectrometry, co-immunoprecipitation, GST pull-down, and ubiquitination assays were used to explore the mechanisms of SET7/9 function in breast cancer. We evaluated the expression of SET7/9 in different breast cancer cohorts and found that higher expression indicated worse survival times in these public databases. We demonstrated positive effects of SET7/9 on cell proliferation, migration, and invasion via the activation of Runt-related transcription factor 2 (RUNX2). We demonstrate that tripartite motif-containing protein 21 (TRIM21) physically associates with SET7/9 and functions as a major negative regulator upstream of SET7/9 through a proteasome-dependent mechanism and increased ubiquitination. Taken together, our data suggest that SET7/9 has a promoting role via the regulation of RUNX2, whereas TRIM21-mediated SET7/9 degradation acts as an anti-braking system in the progression of breast cancer.

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“…A novel in vivo assay combining in situ hybridization and a proximity ligation assay provides further evidence that the H3K4me2 mark at the Myh11 locus is restricted to differentiated SMCs in vivo [68]. Similarly, a histone H3 lysine 4 mono-methylation (H3K4me1) catalysed by the Set7 lysine methyltransferase is considered a further hallmark of transcriptionally active chromatin [69]. Recent transcriptional network analyses has revealed that SMC differentiation genes are also subject to Set7-mediated regulation [69].…”

Section: Epigenetic Control Of Smc Differentiation Genesmentioning

confidence: 99%

“…Similarly, a histone H3 lysine 4 mono-methylation (H3K4me1) catalysed by the Set7 lysine methyltransferase is considered a further hallmark of transcriptionally active chromatin [69]. Recent transcriptional network analyses has revealed that SMC differentiation genes are also subject to Set7-mediated regulation [69]. Hence, several cell-specific epigenetic mechanisms govern the expression of cellular markers during SMC differentiation.…”

Section: Epigenetic Control Of Smc Differentiation Genesmentioning

confidence: 99%

The Dichotomy of Vascular Smooth Muscle Differentiation/De- Differentiation in Health and Disease

Luca¹,

Hakimjavadi²,

Burtenshaw³

et al. 2018

Muscle Cell and Tissue - Current Status of Research Field

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Vascular smooth muscle cells (SMCs) are thought to display cellular plasticity by alternating between a quiescent 'contractile' differentiated phenotype and a proliferative 'synthetic' de-differentiated phenotype in response to induction of distinct developmental pathways or to local micro-environmental cues. This classic de-differentiation and reprogramming process is associated with a significant loss in the expression of key SMC differentiation marker genes for a large number of proliferative vascular diseases in vivo and in sub-cultured cells in vitro. Regarded as essential for vascular regeneration and repair in vivo, phenotypic modulation represents a critical target for therapeutic intervention. However, recent evidence now suggests that this process of vascular regeneration may also involve differentiation of resident vascular stem cells and the accumulation of stem cell-derived myogenic, osteochondrogenic and macrophage-like phenotypes within vascular lesions in vivo and across sub-cultured SMC cell populations in vitro. This review summarises our current knowledge of vascular regeneration, de-differentiation and reprogramming of vascular SMCs, and focuses on the accumulating evidence of a putative role for stem cell-derived progeny and the evolving dichotomy of the origin of SMC-like cells during intimal-medial thickening and the progression of arteriosclerotic disease.

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Set7 mediated interactions regulate transcriptional networks in embryonic stem cells

Cited by 17 publications

References 53 publications

Critical roles of protein methyltransferases and demethylases in the regulation of embryonic stem cell fate

Critical roles of protein methyltransferases and demethylases in the regulation of embryonic stem cell fate

SET7/9 promotes multiple malignant processes in breast cancer development via RUNX2 activation and is negatively regulated by TRIM21

The Dichotomy of Vascular Smooth Muscle Differentiation/De- Differentiation in Health and Disease

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