Evidence map›Paper›PMID 28881656›Full record

ArticleOncotarget2017

BRD4 facilitates DNA damage response and represses CBX5/Heterochromatin protein 1 (HP1).

Georgios Pongas, Marianne K Kim, Dong J Min, Carrie D House, Elizabeth Jordan, Natasha Caplen, Sirisha Chakka, Joyce Ohiri, Michael J Kruhlak, Christina M Annunziata

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

20 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
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  3. The Sound of Silence: Suppressing CBX5 Decreases Fibrosis by Inhibiting Fibroblasts.American journal of respiratory cell and molecular biology · 2025
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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

10 authors at 2 institutions in 1 country.

Georgios Pongas *Women's Malignancies Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA.
Marianne K Kim *Women's Malignancies Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA.
Dong J MinLaboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA.
Carrie D HouseWomen's Malignancies Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA.
Elizabeth JordanWomen's Malignancies Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA.
Natasha CaplenGenetics Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA.
Sirisha ChakkaGenetics Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA.
Joyce OhiriWomen's Malignancies Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA.
Michael J KruhlakExperimental Immunology Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA.
Christina M AnnunziataWomen's Malignancies Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA.
Center for Cancer Research · USNational Cancer Institute · US

Funding

Nuclear Factor-kappaB in Ovarian CancerZIABC011054 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI ANNUNZIATA, CHRISTINA · 2009 to 2023
$12.1M
6 · The paper itself

Abstract

Ovarian cancer (OC) is a heterogeneous disease characterized by defective DNA repair. Very few targets are universally expressed in the high grade serous (HGS) subtype. We previously identified that CHK1 was overexpressed in most of HGSOC. Here, we sought to understand the DNA damage response (DDR) to CHK1 inhibition and increase the anti-tumor activity of this pathway. We found BRD4 suppression either by siRNA or BRD4 inhibitor JQ1 enhanced the cytotoxicity of CHK1 inhibition. Interestingly, BRD4 was amplified and/or upregulated in a subset of HGSOC with statistical correlation to overall survival. BRD4 inhibition increased CBX5 (HP1α) level. CHK1 inhibitor induced DDR marker, γ-H2AX, but BRD4 suppression did not. Furthermore, nuclear localization of CBX5 and γ-H2AX was mutually exclusive in BRD4-and CHK1-inhibited cells, suggesting BRD4 facilitates DDR by repressing CBX5. Our results provide a strong rationale for clinical investigation of CHK1 and BRD4 co-inhibition, especially for HGSOC patients with BRD4 overexpression.

Indexed as

BRD4CBX5CHK1DNA repairheterochromatin

Identifiers

PMID28881656
PMCPMC5584257
OpenAlexW2620466426

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.