Evidence map›Paper›PMID 29333926›Full record

ArticleCancer biology & therapy2018

Engrailed 1 overexpression as a potential prognostic marker in quintuple-negative breast cancer.

Yu Jin Kim, Minjung Sung, Ensel Oh, Michael Van Vrancken, Ji-Young Song, Kyungsoo Jung, Yoon-La Choi

Open access · hybridAbstract read
In one paragraph

Article in Cancer biology & therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

15 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Article
  3. Engrailed-1 Promotes Pancreatic Cancer Metastasis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
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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

7 authors at 2 institutions in 1 country.

Yu Jin Kima Laboratory of Cancer Genomics and Molecular Pathology, Samsung Medical Center, Sungkyunkwan University School of Medicine , Seoul , Korea.
Minjung Sunga Laboratory of Cancer Genomics and Molecular Pathology, Samsung Medical Center, Sungkyunkwan University School of Medicine , Seoul , Korea.
Ensel Ohb Department of Health Sciences and Technology , SAIHST, Sungkyunkwan University , Seoul , Korea.
Michael Van Vranckena Laboratory of Cancer Genomics and Molecular Pathology, Samsung Medical Center, Sungkyunkwan University School of Medicine , Seoul , Korea.
Ji-Young Songa Laboratory of Cancer Genomics and Molecular Pathology, Samsung Medical Center, Sungkyunkwan University School of Medicine , Seoul , Korea.
Kyungsoo Junga Laboratory of Cancer Genomics and Molecular Pathology, Samsung Medical Center, Sungkyunkwan University School of Medicine , Seoul , Korea.
Yoon-La Choia Laboratory of Cancer Genomics and Molecular Pathology, Samsung Medical Center, Sungkyunkwan University School of Medicine , Seoul , Korea.
Samsung Medical Center · KRSungkyunkwan University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Triple-negative breast cancer (TNBC) is an aggressive breast cancer subtype characterized by poor patient prognosis and for which no targeted therapies are currently available. TNBC can be further categorized as either basal-like (BLBC) or quintuple-negative breast cancer (QNBC). In the present study, we aimed to identify novel molecular therapeutic targets for TNBC by analyzing the mRNA expression of TNBC-related genes in publicly available microarray data sets. We found that Engrailed 1 (EN1) was significantly overexpressed in TNBC. Using breast cancer cell lines, we found that EN1 was more highly expressed in TNBC than in other breast cancer subtypes. EN1 expression was analyzed in 199 TNBC paraffin-embedded tissue samples by immunohistochemistry. EN1 protein expression was positively associated with reduced overall survival (OS) rate in patients with QNBC, but not those with BLBC. The importance of EN1 expression in QNBC cell viability and tumorigenicity was evaluated using the QNBC cell lines, HCC38 and HCC1395. Based on our data, EN1 may promote the proliferation, migration, and multinucleation of QNBC cells, likely via the transcriptional activation of HDAC8, UTP11L, and ZIC3. We also demonstrated that actinomycin D effectively inhibits EN1 activity in QNBC cells. The results of the present study suggest that EN1 activity is highly clinically relevant to the survival prognosis of patients with QNBC and EN1 is a promising potential therapeutic target for future QNBC treatment.

Indexed as

Gene Expression Regulation, NeoplasticAdultAgedBiomarkers, TumorBreastCell Line, TumorCell ProliferationDatasets as TopicErb-b2 Receptor Tyrosine KinasesErbB ReceptorsFemaleHistone DeacetylasesHomeodomain ProteinsHumansKeratin-5Middle AgedBiomarkers, TumorEGFR protein, humanEN1 protein, humanERBB2 protein, humanErb-b2 Receptor Tyrosine KinasesErbB ReceptorsHDAC8 protein, humanHistone DeacetylasesHomeodomain ProteinsKeratin-5KRT5 protein, humanReceptors, EstrogenReceptors, ProgesteroneRepressor ProteinsRNA, MessengerTranscription FactorsZIC3 protein, humanBreast cancerEngrailed 1Microarray data and Actinomycin DPrognostic markerQuintuple-negative breast cancerTriple-negative breast cancer

Identifiers

PMID29333926
PMCPMC5902237
OpenAlexW2783653997

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

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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.