EP300-HDAC1-SWI/SNF functional unit defines transcription of some DNA repair enzymes during differentiation of human macrophages

Pietrzak, Julita; Płoszaj, Tomasz; Pułaski, Łukasz; Robaszkiewicz, Agnieszka

doi:10.1016/j.bbagrm.2018.10.019

Cited by 28 publications

(36 citation statements)

References 34 publications

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“…In the current study, we show that BRG1 binding occurs at the promoters of functionally linked genes in proliferating breast cancer cells, revealing a new mechanism by which BRG1 defines gene transcription.Cancers 2020, 12, 349 2 of 17 with the proliferative status of the tumors [2]. Once again, direct molecular and mechanistical mutual interdependence has not been forthcoming.Our recently published results provide evidence that transcription of some of DNA repair genes, such as PARP1, BRCA1, and XRCC1, is controlled by SWI/SNF in a cell cycle-dependent manner [3]. In our model of monocyte-to-macrophage differentiation promoters of DNA repair genes, characterized by the presence of CpG island and E2F motifs, were enriched in SWI/SNF-EP300-HDAC1 complexes.…”

supporting

confidence: 56%

“…Our recently published results provide evidence that transcription of some of DNA repair genes, such as PARP1, BRCA1, and XRCC1, is controlled by SWI/SNF in a cell cycle-dependent manner [3]. In our model of monocyte-to-macrophage differentiation promoters of DNA repair genes, characterized by the presence of CpG island and E2F motifs, were enriched in SWI/SNF-EP300-HDAC1 complexes.…”

supporting

confidence: 56%

“…Lack of reciprocity between enzyme and H3, as well as weak negative co-occurrence with H3K27me3, seem to further confirm a previously postulated mechanism, where BRG1 evicted histones from transcriptionally permissive promoters and enabled gene expression. In human macrophages, BRG1/H3K27ac-positive promoters are characterized by binding motif for E2F (indicative of likely gene dependence on cell cycle status) and/or the CpG island [3]. To test whether distribution of BRG1 is associated with similar chromatin and DNA features in proliferating breast cancer cells, MDA-MB-231, we looked for overlapping regions adjacent to TSS (±2 kbp), which are characterized by the occurrence of BRG1, H3K27ac, E2F motifs, and CpG islands.…”

Section: E2f/cpg Motifs At the Acetylated Gene Promoters Mark Brg1 DImentioning

confidence: 99%

“…Cell cycle progression in MCF7 and MDA-MB-231 cells treated with iCDK4/6, iEP300 and iSWI/SNF for 48 h was analyzed by flow cytometry as described previously [3]. Additionally, protein level of Ki67, PCNA and CCNB was monitored in cell lysates by western blot.…”

Section: Evaluation Of Cell Proliferationmentioning

confidence: 99%

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BRG1 Activates Proliferation and Transcription of Cell Cycle-Dependent Genes in Breast Cancer Cells

Sobczak

Pietrzak

Płoszaj

et al. 2020

Cancers

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Cancer malignancy is usually characterized by unlimited self-renewal. In some types of advanced tumors that are rapidly dividing, gene expression profiles depict elevations in pro-proliferative genes accompanied by coordinately elevated transcription of factors responsible for removal of DNA lesions. In our studies, fast proliferating breast cancer cell lines (MDA-MB-231 and MCF7), BRG1, a component of the SWI/SNF complex, emerges as an activator of functionally-linked genes responsible for activities such as mitotic cell divisions and DNA repair. Products of at least some of them are considerably overrepresented in breast cancer cells and BRG1 facilitates growth of MCF7 and MDA-MB-231 cell lines. BRG1 occurs at the promoters of genes such as CDK4, LIG1, and NEIL3, which are transcriptionally controlled by cell cycle progression and highly acetylated by EP300 in proliferating cells. As previously documented, in dividing cells BRG1 directly activates gene transcription by evicting EP300 modified nucleosomes from the promoters and, thereby, relaxing chromatin. However, the deficiency of BRG1 or EP300 activity for 48 h leads to cell growth arrest and to chromatin compaction, but also to the assembly of RB1/HDAC1/EZH2 complexes at the studied cell cycle-dependent gene promoters. Epigenetic changes include histone deacetylation and accumulation of H3K27me trimethylation, both known to repress transcription. Cell cycle arrest in G1 by inhibition of CDK4/6 phenocopies the effect of the long-term BRG1 inhibition on the chromatin structure. These results suggest that BRG1 may control gene transcription also by promoting expression of genes responsible for cell cycle progression in the studied breast cancer cells. In the current study, we show that BRG1 binding occurs at the promoters of functionally linked genes in proliferating breast cancer cells, revealing a new mechanism by which BRG1 defines gene transcription.

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supporting

confidence: 56%

supporting

confidence: 56%

Section: E2f/cpg Motifs At the Acetylated Gene Promoters Mark Brg1 DImentioning

confidence: 99%

Section: Evaluation Of Cell Proliferationmentioning

confidence: 99%

See 2 more Smart Citations

BRG1 Activates Proliferation and Transcription of Cell Cycle-Dependent Genes in Breast Cancer Cells

Sobczak

Pietrzak

Płoszaj

et al. 2020

Cancers

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“…W połowie tych regionów zidentyfikowano ponadto motyw dla wiązania czynników transkrypcyjnych z rodziny E2F, które łączą aktywność transkrypcyjną genu ze statusem proliferacji komórek. W ludzkich makrofagach oraz komórkach nowotworu piersi dla CpG/E2F-dodatnich promotorów funkcjonalnie powiązanych genów opisano nową jednostkę regulatorową, w skład której wchodzi kompleks SWI/SNF oparty na aktywności BRG1 oraz enzymy -acetylotransferaza EP300 i deacetylaza HDAC1 kontrolujące stopień acetylacji histonów [10,11]. Pierwszy z nich acetyluje reszty histonowe, które w formie zmienionej zostają rozpoznane przez BRG1.…”

Section: Brg1 -Budowa I Funkcjeunclassified

Udział kompleksów SWI/SNF opartych na aktywności BRG1 w determinowaniu fenotypu komórek nowotworowych

2020

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ATP-zależne kompleksy remodelujące chromatynę stanowią ważny element epigenetycznego mechanizmu regulującego transkrypcję. Posiadają one zdolność do wstawiania, usuwania i przesuwania nukleosomów w obrębie elementów regulatorowych genów kontrolując w ten sposób dostępność DNA dla maszynerii transkrypcyjnej. Jednym z czterech zidentyfikowanych i opisanych dotychczas kompleksów jest SWI/SNF, w którym enzymatycznymi „motorami” są białka BRM i BRG1. Rosnąca liczba opublikowanych prac wskazuje na udział BRG1 w patofizjologii niektórych typów nowotworów, ponieważ aktywność tego enzymu odpowiada za ekspresję genów, których produkty odpowiadają za proliferację, naprawę DNA, transport przezbłonowy czy metabolizm. Inhibitory BRG1 i enzymów, które determinują aktywność BRG1 lub znakują histony mające ulec przemieszczeniu przez BRG1 mogą stać się w przyszłości alternatywą dla obecnie stosowanych w terapiach związków hamujących wzrost guzów lub suplementem zwiększającym wrażliwość nowotworów na działanie leków przeciwnowotworowych.

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TRIM25-mediated XRCC1 ubiquitination accelerates atherosclerosis by inducing macrophage M1 polarization and programmed death

Wu,

Gao,

et al. 2024

Inflamm. Res.

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EP300-HDAC1-SWI/SNF functional unit defines transcription of some DNA repair enzymes during differentiation of human macrophages

Cited by 28 publications

References 34 publications

BRG1 Activates Proliferation and Transcription of Cell Cycle-Dependent Genes in Breast Cancer Cells

BRG1 Activates Proliferation and Transcription of Cell Cycle-Dependent Genes in Breast Cancer Cells

Udział kompleksów SWI/SNF opartych na aktywności BRG1 w determinowaniu fenotypu komórek nowotworowych

TRIM25-mediated XRCC1 ubiquitination accelerates atherosclerosis by inducing macrophage M1 polarization and programmed death

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