Evidence map›Paper›PMID 28678170›Full record

ArticleInternational journal of molecular sciences2017

Differential Effects of Histone Acetyltransferase GCN5 or PCAF Knockdown on Urothelial Carcinoma Cells.

Evangelia A Koutsogiannouli, Nicholas Wagner, Christiane Hader, Maria Pinkerneil, Michèle J Hoffmann, Wolfgang A Schulz

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

19 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
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  6. Integrative analysis of histone acetyltransferase KAT2A in human cancer.Cancer biomarkers : section A of Disease markers · 2023
    Article
  7. Article
  8. Review
  9. Complex functions of Gcn5 and Pcaf in development and disease.Biochimica et biophysica acta. Gene regulatory mechanisms · 2021
    Review
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  11. Review
  12. Article
  13. Review
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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

6 authors at 1 institution in 1 country.

Evangelia A KoutsogiannouliDepartment of Urology, Heinrich Heine University, 40225 Düsseldorf, Germany. evkouts@gmail.com.
Nicholas WagnerDepartment of Urology, Heinrich Heine University, 40225 Düsseldorf, Germany. nicholas.wagner@hhu.de.
Christiane HaderDepartment of Urology, Heinrich Heine University, 40225 Düsseldorf, Germany. christiane.hader@hhu.de.
Maria PinkerneilDepartment of Urology, Heinrich Heine University, 40225 Düsseldorf, Germany. maria.lehmann@hhu.de.
Michèle J HoffmannDepartment of Urology, Heinrich Heine University, 40225 Düsseldorf, Germany. michele.hoffmann@hhu.de.
Wolfgang A SchulzDepartment of Urology, Heinrich Heine University, 40225 Düsseldorf, Germany. wolfgang.schulz@hhu.de.
Heinrich Heine University Düsseldorf · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Disturbances in histone acetyltransferases (HATs) are common in cancers. In urothelial carcinoma (UC), p300 and CBP are often mutated, whereas the GNAT family HATs GCN5 and PCAF (General Control Nonderepressible 5, p300/CBP-Associated Factor) are often upregulated. Here, we explored the effects of specific siRNA-mediated knockdown of GCN5, PCAF or both in four UC cell lines (UCCs). Expression of various HATs and marker proteins was measured by qRT-PCR and western blot. Cellular effects of knockdowns were analyzed by flow cytometry and ATP-, caspase-, and colony forming-assays. GCN5 was regularly upregulated in UCCs, whereas PCAF was variable. Knockdown of GCN5 or both GNATs, but not of PCAF alone, diminished viability and inhibited clonogenic growth in 2/4 UCCs, inducing cell cycle changes and caspase-3/7 activity. PCAF knockdown elicited GCN5 mRNA upregulation. Double knockdown increased c-MYC and MDM2 (Mouse Double Minute 2) in most cell lines. In conclusion, GCN5 upregulation is especially common in UCCs. GCN5 knockdown impeded growth of specific UCCs, whereas PCAF knockdown elicited minor effects. The limited sensitivity towards GNAT knockdown and its variation between the cell lines might be due to compensatory effects including HAT, c-MYC and MDM2 upregulation. Our results predict that developing drugs targeting individual HATs for UC treatment may be challenging.

Indexed as

ApoptosisBiomarkers, TumorCarcinomaCell Line, TumorCell SurvivalCellular SenescenceGene ExpressionGene Knockdown TechniquesHumansp300-CBP-Associated Factorp300-CBP Transcription FactorsProtein BindingRNA InterferenceRNA, MessengerRNA, Small InterferingUrethral NeoplasmsBiomarkers, Tumorp300-CBP-Associated Factorp300-CBP Transcription FactorsRNA, MessengerRNA, Small Interferingbladder cancerCBPc-MYCepigenetic drugsGCN5histone acetyltransferasesMDM2p300PCAFurothelial carcinoma

Identifiers

PMID28678170
PMCPMC5535940
OpenAlexW2731960028

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.