ArticleMolecular and cellular biology2013
BRG1 is required for formation of senescence-associated heterochromatin foci induced by oncogenic RAS or BRCA1 loss.
Article in Molecular and cellular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
26 citing papers in PubMed, 46 citations in OpenAlex.
- The controversial role of senescence-associated secretory phenotype (SASP) in cancer therapy.Molecular cancer · 2025Review
- The role of SMARCA4 in lung cancer.Scientific reports · 2025Review
- Regulation of cellular senescence in tumor progression and therapeutic targeting: mechanisms and pathways.Molecular cancer · 2025Review
- BRG1: Promoter or Suppressor of Cancer? The Outcome of BRG1's Interaction with Specific Cellular Pathways.International journal of molecular sciences · 2023Review
- BRCA1 heterozygosity promotes DNA damage-induced senescence in a sex-specific manner following repeated mild traumatic brain injury.Frontiers in neuroscience · 2023Article
- GermlineJCO precision oncology · 2022Article
- Molecular dissection on inhibition of Ras-induced cellular senescence by small t antigen of SV40.Cellular and molecular life sciences : CMLS · 2022Article
- HSP90 Inhibitor Ganetespib Enhances the Sensitivity of Mantle Cell Lymphoma to Bruton's Tyrosine Kinase Inhibitor Ibrutinib.Frontiers in pharmacology · 2022Article
- Brahma-related gene-1 promotes tubular senescence and renal fibrosis through Wnt/β-catenin/autophagy axis.Clinical science (London, England : 1979) · 2021Article
- Breast cancer type 1 and neurodegeneration: consequences of deficient DNA repair.Brain communications · 2021Review
- Interleukin-1β Drives Cellular Senescence of Rat Astrocytes Induced by Oligomerized Amyloid β Peptide and Oxidative Stress.Frontiers in neurology · 2020Article
- Roles of MYC-targeting long non-coding RNA MINCR in cell cycle regulation and apoptosis in non-small cell lung Cancer.Respiratory research · 2019Article
- Article
- RIPK1 suppresses apoptosis mediated by TNF and caspase-3 in intervertebral discs.Journal of translational medicine · 2019Article
- Review
- A CRISPR knockout screen identifies SETDB1-target retroelement silencing factors in embryonic stem cells.Genome research · 2018Article
- Epigenetic regulation in cell senescence.Journal of molecular medicine (Berlin, Germany) · 2017Review
- The Role of p16International journal of molecular sciences · 2017Review
- The Histone Variant MacroH2A1 Is a BRCA1 Ubiquitin Ligase Substrate.Cell reports · 2017Article
- p16 loss rescues functional decline of Brca1-deficient mammary stem cells.Cell cycle (Georgetown, Tex.) · 2017Article
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Cellular senescence is an important tumor suppression mechanism. We have previously reported that both oncogene-induced dissociation of BRCA1 from chromatin and BRCA1 knockdown itself drive senescence by promoting formation of senescence-associated heterochromatin foci (SAHF). However, the molecular mechanism by which BRCA1 regulates SAHF formation and senescence is unclear. BRG1 is a chromatin-remodeling factor that interacts with BRCA1 and pRB. Here we show that BRG1 is required for SAHF formation and senescence induced by oncogenic RAS or BRCA1 loss. The interaction between BRG1 and BRCA1 is disrupted during senescence. This correlates with an increased level of chromatin-associated BRG1 in senescent cells. BRG1 knockdown suppresses the formation of SAHF and senescence, while it has no effect on BRCA1 chromatin dissociation induced by oncogenic RAS, indicating that BRG1 functions downstream of BRCA1 chromatin dissociation. Furthermore, BRG1 knockdown inhibits SAHF formation and senescence induced by BRCA1 knockdown. Conversely, BRG1 overexpression drives SAHF formation and senescence in a DNA damage-independent manner. This effect depends upon BRG1's chromatin-remodeling activity as well as the interaction between BRG1 and pRB. Indeed, the interaction between BRG1 and pRB is enhanced during senescence. Chromatin immunoprecipitation analysis revealed that BRG1's association with the human CDKN2A and CDKN1A gene promoters was enhanced during senescence induced by oncogenic RAS or BRCA1 knockdown. Consistently, knockdown of pRB, p21(CIP1), and p16(INK4a), but not p53, suppressed SAHF formation induced by BRG1. Together, these studies reveal the molecular underpinning by which BRG1 acts downstream of BRCA1 to promote SAHF formation and senescence.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.