Evidence map›Paper›PMID 23698071›Full record

ArticleThe Journal of investigative dermatology2013

Selective inhibition of p300 HAT blocks cell cycle progression, induces cellular senescence, and inhibits the DNA damage response in melanoma cells.

Gai Yan, Mark S Eller, Courtney Elm, Cecilia A Larocca, Byungwoo Ryu, Izabela P Panova, Beverley M Dancy, Erin M Bowers, David Meyers, Lisa Lareau and 3 more

Open access · greenAbstract read
In one paragraph

Article in The Journal of investigative dermatology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
4.6field-weighted citation impact, top 4% 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

67 citing papers in PubMed, 132 citations in OpenAlex.

  1. Review
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  17. Review
  18. Article
  19. Drugging the Epigenome: Overcoming Resistance to Targeted and Immunotherapies in Melanoma.JID innovations : skin science from molecules to population health · 2022
    Review
  20. HDAC2 Is Involved in the Regulation of BRN3A in Melanocytes and Melanoma.International journal of molecular sciences · 2022
    Article

7 more citing papers are in PubMed but not listed here.

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

13 authors at 3 institutions in 1 country.

Gai YanDepartment of Oncology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Mark S EllerDepartment of Dermatology, Boston University School of Medicine, Boston, Massachusetts, USA.
Courtney ElmDepartment of Dermatology, Boston University School of Medicine, Boston, Massachusetts, USA.
Cecilia A LaroccaDepartment of Oncology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Byungwoo RyuDepartment of Dermatology, Boston University School of Medicine, Boston, Massachusetts, USA.
Izabela P PanovaDepartment of Dermatology, Boston University School of Medicine, Boston, Massachusetts, USA.
Beverley M DancyDepartment of Pharmacology and Molecular Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Erin M BowersDepartment of Pharmacology and Molecular Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
David MeyersDepartment of Pharmacology and Molecular Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Lisa LareauDepartment of Oncology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Philip A ColeDepartment of Pharmacology and Molecular Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. Electronic address: pcole@jhmi.edu.
Sean D TavernaDepartment of Pharmacology and Molecular Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. Electronic address: staverna@jhmi.edu.
Rhoda M AlaniDepartment of Oncology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA; Department of Dermatology, Boston University School of Medicine, Boston, Massachusetts, USA; Department of Pharmacology and Molecular Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. Electronic address: alani@bu.edu.
Johns Hopkins University · USBoston University · USJohns Hopkins Medicine · US

Funding

Translational Research Central ServicesP30CA006973 · NCI · JOHNS HOPKINS UNIVERSITY · PI Rosalie Wollett · 1985 to 2026
$208.6M
Networks, Pathways and Dynamics of Lysine ModificationU54GM103520 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI BADER, JOEL S. · 2012 to 2013
$7.0M
Mechanisms &Inhibition of Histone AcetyltransferasesR01GM062437 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI COLE, PHILIP A · 2001 to 2012
$3.8M
Defining the role of Id1 in melanoma developmentR01CA107017 · NCI · JOHNS HOPKINS UNIVERSITY · PI ALANI, RHODA M · 2004 to 2008
$1.3M
NCI NIH HHS P30 CA006973NCI NIH HHS R01 CA107017NIGMS NIH HHS R01 GM062437NIGMS NIH HHS U54 GM103520
6 · The paper itself

Abstract

Epigenetic events, including covalent post-translational modifications of histones, have been demonstrated to have critical roles in tumor development and progression. The transcriptional coactivator p300/CBP possesses both histone acetyltransferase (HAT) activity and scaffolding properties that directly influence the transcriptional activation of targeted genes. We have used a potent and specific inhibitor of p300/CBP HAT activity, C646, in order to evaluate the functional contributions of p300/CBP HAT to tumor development and progression. Here we report that C646 inhibits the growth of human melanoma and other tumor cells and promotes cellular senescence. Global assessment of the p300 HAT transcriptome in human melanoma identified functional roles in promoting cell cycle progression, chromatin assembly, and activation of DNA repair pathways through direct transcriptional regulatory mechanisms. In addition, C646 is shown to promote sensitivity to DNA damaging agents, leading to the enhanced apoptosis of melanoma cells after combination treatment with cisplatin. Together, our data suggest that p300 HAT activity mediates critical growth regulatory pathways in tumor cells and may serve as a potential therapeutic target for melanoma and other malignancies by promoting cellular responses to DNA damaging agents that are currently ineffective against specific cancers.

Indexed as

ApoptosisBenzoatesCell CycleCell Line, TumorCellular SenescenceDNA DamageEnzyme InhibitorsEpigenesis, GeneticHistone AcetyltransferasesHumansMelanomaNitrobenzenesp300-CBP-Associated Factorp300-CBP Transcription FactorsPyrazolesPyrazolones4-(4-((5-(4,5-dimethyl-2-nitrophenyl)-2-furanyl)methylene)-4,5-dihydro-3-methyl-5-oxo-1H-pyrazol-1-yl)benzoic acidBenzoatesEnzyme InhibitorsHistone AcetyltransferasesNitrobenzenesp300-CBP-Associated Factorp300-CBP Transcription FactorsPyrazolesPyrazolones

Identifiers

PMID23698071
PMCPMC4380234
OpenAlexW2031875849

What OpenQuestion holds

Textmetadata
LicenceTDM
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.