Evidence map›Paper›PMID 32458023›Full record

ArticleCellular and molecular life sciences : CMLS2021

Ubiquitin chromatin remodelling after DNA damage is associated with the expression of key cancer genes and pathways.

Alexander J Cole, Kristie-Ann Dickson, Christopher Liddle, Clare Stirzaker, Jaynish S Shah, Roderick Clifton-Bligh, Deborah J Marsh

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.9field-weighted citation impact, top 27% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. PARP1 modulates METTL3 promoter chromatin accessibility and associated LPAR5 RNA mMolecular therapy : the journal of the American Society of Gene Therapy · 2023
    Article
  7. Article
  8. Article
  9. Emerging Roles of Non-proteolytic Ubiquitination in Tumorigenesis.Frontiers in cell and developmental biology · 2022
    Review
  10. Review
  11. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 2 countries.

Alexander J ColeHormones and Cancer Group, Kolling Institute of Medical Research, Royal North Shore Hospital, University of Sydney, Sydney, NSW, Australia.
Kristie-Ann DicksonHormones and Cancer Group, Kolling Institute of Medical Research, Royal North Shore Hospital, University of Sydney, Sydney, NSW, Australia.
Christopher LiddleStorr Liver Centre, Westmead Institute for Medical Research and Sydney Medical School, University of Sydney, Sydney, NSW, Australia.
Clare StirzakerEpigenetics Research Laboratory, Genomics and Epigenetics Division, Garvan Institute of Medical Research, UNSW, Sydney, NSW, Australia.
Jaynish S ShahHormones and Cancer Group, Kolling Institute of Medical Research, Royal North Shore Hospital, University of Sydney, Sydney, NSW, Australia.
Roderick Clifton-BlighHormones and Cancer Group, Kolling Institute of Medical Research, Royal North Shore Hospital, University of Sydney, Sydney, NSW, Australia.
Deborah J MarshHormones and Cancer Group, Kolling Institute of Medical Research, Royal North Shore Hospital, University of Sydney, Sydney, NSW, Australia. Deborah.Marsh@uts.edu.au.ORCID http://orcid.org/0000-0001-5899-4931
The University of Sydney · AUUniversity of Technology Sydney · AUGarvan Institute of Medical Research · AU

Funding

Australian Research Council FT100100489Cancer Council NSW RG13-10National Health and Medical Research Council APP1004799
6 · The paper itself

Abstract

Modification of the cancer-associated chromatin landscape in response to therapeutic DNA damage influences gene expression and contributes to cell fate. The central histone mark H2Bub1 results from addition of a single ubiquitin on lysine 120 of histone H2B and is an important regulator of gene expression. Following treatment with a platinum-based chemotherapeutic, there is a reduction in global levels of H2Bub1 accompanied by an increase in levels of the tumor suppressor p53. Although total H2Bub1 decreases following DNA damage, H2Bub1 is enriched downstream of transcription start sites of specific genes. Gene-specific H2Bub1 enrichment was observed at a defined group of genes that clustered into cancer-related pathways and correlated with increased gene expression. H2Bub1-enriched genes encompassed fifteen p53 target genes including PPM1D, BTG2, PLK2, MDM2, CDKN1A and BBC3, genes related to ERK/MAPK signalling, those participating in nucleotide excision repair including XPC, and genes involved in the immune response and platinum drug resistance including POLH. Enrichment of H2Bub1 at key cancer-related genes may function to regulate gene expression and influence the cellular response to therapeutic DNA damage.

Indexed as

bcl-2-Associated X ProteinCell Line, TumorChromatinChromatin Assembly and DisassemblyCisplatinCyclin-Dependent Kinase Inhibitor p21DNA DamageGene Expression Regulation, NeoplasticHumansMutagenesis, Site-DirectedNeoplasmsProto-Oncogene Proteins c-mdm2Signal TransductionTranscription Initiation SiteTumor Suppressor Protein p53Ubiquitinationbcl-2-Associated X ProteinCDKN1A protein, humanChromatinCisplatinCyclin-Dependent Kinase Inhibitor p21Proto-Oncogene Proteins c-mdm2TP53 protein, humanTumor Suppressor Protein p53CisplatinDNA damageH2Bub1Histone modificationMonoubiquitinationp53

Identifiers

PMID32458023
PMCPMC11072370
OpenAlexW3030284169

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.