Evidence map›Paper›PMID 34403195›Full record

ArticleEMBO reports2021

BAZ2A-mediated repression via H3K14ac-marked enhancers promotes prostate cancer stem cells.

Rodrigo Peña-Hernández, Rossana Aprigliano, Sandra Carina Frommel, Karolina Pietrzak, Seraina Steiger, Marcin Roganowicz, Luigi Lerra, Juliana Bizzarro, Raffaella Santoro

Open access · greenAbstract read
In one paragraph

Article in EMBO reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

25 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
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  9. Enhanced cellular death in liver and breast cancer cells by dual BET/BRPF1 inhibitors.Protein science : a publication of the Protein Society · 2024
    Article
  10. Article
  11. Article
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  13. Review
  14. Reevaluation of bromodomain ligands targeting BAZ2A.Protein science : a publication of the Protein Society · 2023
    Article
  15. Article
  16. Review
  17. Article
  18. Article
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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

9 authors at 1 institution in 1 country.

Rodrigo Peña-HernándezDepartment of Molecular Mechanisms of Disease, DMMD, University of Zurich, Zurich, Switzerland.
Rossana ApriglianoDepartment of Molecular Mechanisms of Disease, DMMD, University of Zurich, Zurich, Switzerland.ORCID 0000-0001-8537-122X
Sandra Carina FrommelDepartment of Molecular Mechanisms of Disease, DMMD, University of Zurich, Zurich, Switzerland.
Karolina PietrzakDepartment of Molecular Mechanisms of Disease, DMMD, University of Zurich, Zurich, Switzerland.
Seraina SteigerDepartment of Molecular Mechanisms of Disease, DMMD, University of Zurich, Zurich, Switzerland.
Marcin RoganowiczDepartment of Molecular Mechanisms of Disease, DMMD, University of Zurich, Zurich, Switzerland.
Luigi LerraDepartment of Molecular Mechanisms of Disease, DMMD, University of Zurich, Zurich, Switzerland.
Juliana BizzarroDepartment of Molecular Mechanisms of Disease, DMMD, University of Zurich, Zurich, Switzerland.
Raffaella SantoroDepartment of Molecular Mechanisms of Disease, DMMD, University of Zurich, Zurich, Switzerland.ORCID 0000-0001-9894-2896
University of Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prostate cancer (PCa) is one of the most prevalent cancers in men. Cancer stem cells are thought to be associated with PCa relapse. Here, we show that BAZ2A is required for PCa cells with a cancer stem-like state. BAZ2A genomic occupancy in PCa cells coincides with H3K14ac-enriched chromatin regions. This association is mediated by BAZ2A-bromodomain (BAZ2A-BRD) that specifically binds H3K14ac. BAZ2A associates with inactive enhancers marked by H3K14ac and repressing transcription of genes frequently silenced in aggressive and poorly differentiated PCa. BAZ2A-mediated repression is also linked to EP300 that acetylates H3K14ac. BAZ2A-BRD mutations or treatment with inhibitors abrogating BAZ2A-BRD/H3K14ac interaction impair PCa stem cells. Furthermore, pharmacological inactivation of BAZ2A-BRD impairs Pten-loss oncogenic transformation of prostate organoids. Our findings indicate a role of BAZ2A-BRD in PCa stem cell features and suggest potential epigenetic-reader therapeutic strategies to target BAZ2A in aggressive PCa.

Indexed as

ProstateProstatic NeoplasmsBromodomain Containing ProteinsCell Line, TumorChromatinChromosomal Proteins, Non-HistoneHumansMaleNeoplasm Recurrence, LocalNeoplastic Stem CellsOncogenesBAZ2A protein, humanBromodomain Containing ProteinsChromatinChromosomal Proteins, Non-HistoneBAZ2AbromodomainchromatinH3K14acprostate cancer

Identifiers

PMID34403195
PMCPMC8567280
OpenAlexW3195764989

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.