Evidence map›Paper›PMID 27081696›Full record

ArticleOncotarget2016

Epigenetic reader BRD4 inhibition as a therapeutic strategy to suppress E2F2-cell cycle regulation circuit in liver cancer.

Seong Hwi Hong, Jung Woo Eun, Sung Kyung Choi, Qingyu Shen, Wahn Soo Choi, Jeung-Whan Han, Suk Woo Nam, Jueng Soo You

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

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

28 citing papers in PubMed, 63 citations in OpenAlex.

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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

8 authors at 3 institutions in 1 country.

Seong Hwi HongKonkuk University Medical Center, School of Medicine, Konkuk University, Seoul 143-701, Korea.
Jung Woo EunFunctional RNomics Research Center, College of Medicine, The Catholic University, Seoul 137-701, Korea.
Sung Kyung ChoiKonkuk University Medical Center, School of Medicine, Konkuk University, Seoul 143-701, Korea.
Qingyu ShenFunctional RNomics Research Center, College of Medicine, The Catholic University, Seoul 137-701, Korea.
Wahn Soo ChoiKonkuk University Medical Center, School of Medicine, Konkuk University, Seoul 143-701, Korea.
Jeung-Whan HanResearch Center for Epigenome Regulation, School of Pharmacy, Sungkyunkwan University, Suwon 440-746, Korea.
Suk Woo NamFunctional RNomics Research Center, College of Medicine, The Catholic University, Seoul 137-701, Korea.
Jueng Soo YouKonkuk University Medical Center, School of Medicine, Konkuk University, Seoul 143-701, Korea.
Konkuk University Medical Center · KRCatholic University of Korea · KRSungkyunkwan University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Deregulation of the epigenome component affects multiple pathways in the cancer phenotype since the epigenome acts at the pinnacle of the hierarchy of gene expression. Pioneering work over the past decades has highlighted that targeting enzymes or proteins involved in the epigenetic regulation is a valuable approach to cancer therapy. Very recent results demonstrated that inhibiting the epigenetic reader BRD4 has notable efficacy in diverse cancer types. We investigated the potential of BRD4 as a therapeutic target in liver malignancy. BRD4 was overexpressed in three different large cohort of hepatocellular carcinoma (HCC) patients as well as in liver cancer cell lines. BRD4 inhibition by JQ1 induced anti-tumorigenic effects including cell cycle arrest, cellular senescence, reduced wound healing capacity and soft agar colony formation in liver cancer cell lines. Notably, BRD4 inhibition caused MYC-independent large-scale gene expression changes in liver cancer cells. Serial gene expression analyses with SK-Hep1 liver cancer cells treated with JQ1 to delineate the key player of BRD4 inhibition identified E2F2 as the first line of downstream direct target of BRD4. Further experiments including chromatin immunoprecipitation (ChIP) assay and loss of function study confirmed E2F2 as key player of BRD4 inhibition. Overexpressed E2F2 is a crucial center of cell cycle regulation and high expression of E2F2 is significantly associated with poor prognosis of HCC patients. Our findings reveal BRD4-E2F2-cell cycle regulation as a novel molecular circuit in liver cancer and provide a therapeutic strategy and innovative insights for liver cancer therapies.

Indexed as

AzepinesBromodomain Containing ProteinsCarcinoma, HepatocellularCell Cycle CheckpointsCell Cycle ProteinsCell Line, TumorCell ProliferationE2F2 Transcription FactorEpigenesis, GeneticHep G2 CellsHumansLiver NeoplasmsNuclear ProteinsTranscription FactorsTriazolesAzepinesBRD4 protein, humanBromodomain Containing ProteinsCell Cycle ProteinsE2F2 protein, humanE2F2 Transcription Factor(+)-JQ1 compoundNuclear ProteinsTranscription FactorsTriazolesBET proteinE2Fepigenetic componentshepatocellular carcinoma (HCC)JQ1

Identifiers

PMID27081696
PMCPMC5078039
OpenAlexW2339081537

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.