Evidence map›Paper›PMID 24998263›Full record

ArticleBMB reports2015

P42 Ebp1 functions as a tumor suppressor in non-small cell lung cancer.

Hyo Rim Ko, Truong Lx Nguyen, Chung Kwon Kim, Youngbin Park, Kyung-Hoon Lee, Jee-Yin Ahn

Open access · goldAbstract read
In one paragraph

Article in BMB reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.3field-weighted citation impact, top 10% 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

13 citing papers in PubMed, 27 citations in OpenAlex.

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  6. The expression and prognostic role of EBP1 and relationship with AR in HER2+ breast cancer.Virchows Archiv : an international journal of pathology · 2020
    Article
  7. Roles of ErbB3-binding protein 1 (EBP1) in embryonic development and gene-silencing control.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  8. Article
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  12. High expression of ErbB3 binding protein 1 (EBP1) predicts poor prognosis of pancreatic ductal adenocarcinoma (PDAC).Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    Article
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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 2 institutions in 2 countries.

Hyo Rim KoDepartment of Molecular Cell Biology; Center for Molecular Medicine, Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Suwon 440-746, Korea.
Truong Lx NguyenDepartment of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Suwon 440-746, Korea.
Chung Kwon KimDepartment of Molecular Cell Biology; Center for Molecular Medicine, Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Suwon 440-746, Korea.
Youngbin ParkDepartment of Biology, Johns Hopkins University, Baltimore, MD 21218, USA.
Kyung-Hoon LeeAnatomy; Center for Molecular Medicine, Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Suwon 440-746, Korea.
Jee-Yin AhnDepartment of Molecular Cell Biology; Center for Molecular Medicine, Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Suwon 440-746, Korea.
Johns Hopkins University · USSungkyunkwan University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although the short isoform of ErbB3-binding protein 1 (Ebp1), p42 has been considered to be a potent tumor suppressor in a number of human cancers, whether p42 suppresses tumorigenesis of lung cancer cells has never been clarified. In the current study we investigated the tumor suppressor role of p42 in non-small cell lung cancer cells. Our data suggest that the expression level of p42 is inversely correlated with the cancerous properties of NSCLC cells and that ectopic expression of p42 is sufficient to inhibit cell proliferation, anchorage-independent growth, and invasion as well as tumor growth in vivo. Interestingly, p42 suppresses Akt activation and overexpression of a constitutively active form of Akt restores the tumorigenic activity of A549 cells that is ablated by exogenous p42 expression. Thus, we propose that p42 Ebp1 functions as a potent tumor suppressor of NSCLC through interruption of Akt signaling.

Indexed as

Genes, Tumor SuppressorAdaptor Proteins, Signal TransducingApoptosisCarcinoma, Non-Small-Cell LungCell Line, TumorErbB ReceptorsHumansLung NeoplasmsRNA-Binding ProteinsSignal TransductionAdaptor Proteins, Signal TransducingErbB ReceptorsPA2G4 protein, humanRNA-Binding Proteins

Identifiers

PMID24998263
PMCPMC4453029
OpenAlexW2081401789

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.