Evidence map›Paper›PMID 21478903›Full record

ArticleOncogene2011

Oncogenic role of EAPII in lung cancer development and its activation of the MAPK-ERK pathway.

C Li, S Fan, T K Owonikoko, F R Khuri, S-Y Sun, R Li

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

25 citing papers in PubMed, 36 citations in OpenAlex.

  1. Trial
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  5. Molecular mechanisms of topoisomerase 2 DNA-protein crosslink resolution.Cellular and molecular life sciences : CMLS · 2020
    Review
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  7. New fluorescence-based high-throughput screening assay for small molecule inhibitors of tyrosyl-DNA phosphodiesterase 2 (TDP2).European journal of pharmaceutical sciences : official journal of the European Federation for Pharmaceutical Sciences · 2018
    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 1 institution in 1 country.

C LiWinship Cancer Institute, Department of Hematology and Medical Oncology, School of Medicine, Emory University, Atlanta, GA, USA.
S Fan
T K Owonikoko
F R Khuri
S-Y Sun
R Li
Emory University · US

Funding

Enhancing the mTOR-targeted cancer therapyR01CA118450 · NCI · EMORY UNIVERSITY · PI SUN, SHI-YONG · 2006 to 2015
$2.6M
Novel systemic therapy to improve clinical outcome in small cell lung cancerK23CA164015 · NCI · EMORY UNIVERSITY · PI OWONIKOKO, TAOFEEK K · 2011 to 2015
$815k
Modulation of EMT by ETS1 and EAPIIK22CA109577 · NCI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI LI, RUNZHAO · 2004 to 2006
$470k
NCI NIH HHS K22 CA109577NCI NIH HHS K22CA109577NCI NIH HHS K23 CA164015NCI NIH HHS R01 CA118450NCI NIH HHS R01CA118450
6 · The paper itself

Abstract

Cancer progression involves multiple complex and interdependent steps, including progressive proliferation, angiogenesis and metastases. The complexity of these processes requires a comprehensive elucidation of the integrated signaling networks for better understanding. EAPII interacts with multiple cancer-related proteins, but its biological significance in cancer development remains unknown. In this report we identified the elevated level of EAPII protein in non-small-cell lung carcinoma (NSCLC) patients and NSCLC cell lines in culture. The oncogenic role of EAPII in lung cancer development was demonstrated using NSCLC cells with genetic manipulations that influence EAPII expression: EAPII overexpression increases proliferation of NSCLC cells with an accelerated transition of cell cycle and facilitates xenograft tumor growth in vivo; EAPII knockdown results in apoptosis of NSCLC cells and reduces xenograft tumor formation. To further explore the mechanism of EAPII's oncogenic role in lung cancer development and to elucidate the potential signaling pathway(s) that EAPII may impact, we employed antibody array to investigate the alternation of the major signaling pathways in NSCLC cells with altered EAPII level. We found that EAPII overexpression significantly activated Raf1 and ERK1/2, but not c-Jun N-terminal kinase and p38 pathways. Consistently, the protein and mRNA levels of MYC and cyclin D1, which are targets of the mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK-ERK) pathway, are significantly increased by EAPII overexpression. Taken together, we demonstrated that EAPII is an oncogenic factor and the activation of MAPK-ERK signaling pathway by EAPII may contribute to lung cancer development.

Indexed as

ApoptosisCarcinoma, Non-Small-Cell LungCell Line, TumorCell ProliferationDNA-Binding ProteinsEnzyme ActivationGene Knockdown TechniquesHumansLung NeoplasmsMitogen-Activated Protein Kinase KinasesNuclear ProteinsOncogenesPhosphoric Diester HydrolasesTranscription FactorsDNA-Binding ProteinsMitogen-Activated Protein Kinase KinasesNuclear ProteinsPhosphoric Diester HydrolasesTDP2 protein, humanTranscription Factors

Identifiers

PMID21478903
PMCPMC3220271
OpenAlexW2053863124

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.