Evidence map›Paper›PMID 23659968›Full record

ArticleClinical cancer research : an official journal of the American Association for Cancer Research2013

ETS2 mediated tumor suppressive function and MET oncogene inhibition in human non-small cell lung cancer.

Mohamed Kabbout, Melinda M Garcia, Junya Fujimoto, Diane D Liu, Denise Woods, Chi-Wan Chow, Gabriela Mendoza, Amin A Momin, Brian P James, Luisa Solis and 4 more

Open access · greenAbstract read
In one paragraph

Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
102citing papers in PubMed, 1 pooled it
3.5field-weighted citation impact, top 7% 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

102 citing papers in PubMed, 1 synthesis or guideline pooled it, 191 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. ETS‑1/ETS‑2 transcription factors in CVD (Review).International journal of molecular medicine · 2026
    Review
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42 more citing papers are in PubMed but not listed here.

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

14 authors at 1 institution in 1 country.

Mohamed KabboutDepartment of Thoracic/Head and Neck Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Melinda M GarciaDepartment of Thoracic/Head and Neck Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Junya FujimotoDepartment of Thoracic/Head and Neck Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Diane D LiuDepartment of Biostatistics, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Denise WoodsDepartment of Thoracic/Head and Neck Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Chi-Wan ChowDepartment of Thoracic/Head and Neck Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Gabriela MendozaDepartment of Thoracic/Head and Neck Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Amin A MominDepartment of Bioinformatics, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Brian P JamesDepartment of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Luisa SolisDepartment of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Carmen BehrensDepartment of Thoracic/Head and Neck Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
J Jack LeeDepartment of Biostatistics, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Ignacio I Wistuba *Department of Thoracic/Head and Neck Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Humam Kadara *Department of Thoracic/Head and Neck Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
The University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
UNIVERSITY OF TEXAS--SPORE IN LUNG CANCERP50CA070907 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI GIBBONS, DON LYNN · 1996 to 2024
$57.4M
NCI NIH HHS CA-16672NCI NIH HHS P30 CA016672NCI NIH HHS P50 CA070907NCI NIH HHS P50CA70907
6 · The paper itself

Abstract

purposeThe ETS2 transcription factor is an evolutionarily conserved gene that is deregulated in cancer. We analyzed the transcriptome of lung adenocarcinomas and normal lung tissue by expression profiling and found that ETS2 was significantly downregulated in adenocarcinomas. In this study, we probed the yet unknown functional role of ETS2 in lung cancer pathogenesis. EXPERIMENTAL

designLung adenocarcinomas (n = 80) and normal lung tissues (n = 30) were profiled using the Affymetrix Human Gene 1.0 ST platform. Immunohistochemical (IHC) analysis was conducted to determine ETS2 protein expression in non-small cell lung cancer (NSCLC) histologic tissue specimens (n = 201). Patient clinical outcome, based on ETS2 IHC expression, was statistically assessed using the log-rank and Kaplan-Meier tests. RNA interference and overexpression strategies were used to assess the effects of ETS2 expression on the transcriptome and on various malignant phenotypes.

resultsETS2 expression was significantly reduced in lung adenocarcinomas compared with normal lung (P < 0.001). Low ETS2 IHC expression was a significant predictor of shorter time to recurrence in NSCLC (P = 0.009, HR = 1.89) and adenocarcinoma (P = 0.03, HR = 1.86). Moreover, ETS2 was found to significantly inhibit lung cancer cell growth, migration, and invasion (P < 0.05), and microarray and pathways analysis revealed significant (P < 0.001) activation of the HGF pathway following ETS2 knockdown. In addition, ETS2 was found to suppress MET phosphorylation and knockdown of MET expression significantly attenuated (P < 0.05) cell invasion mediated by ETS2-specific siRNA. Furthermore, knockdown of ETS2 augmented HGF-induced MET phosphorylation, cell migration, and invasion. CONCLUSION(S): Our findings point to a tumor suppressor role for ETS2 in human NSCLC pathogenesis through inhibition of the MET proto-oncogene.

Indexed as

Carcinoma, Non-Small-Cell LungCell Line, TumorCell MovementCell ProliferationCluster AnalysisGene Expression ProfilingGene Expression Regulation, NeoplasticGene Knockdown TechniquesHepatocyte Growth FactorHumansLung NeoplasmsNeoplasm InvasivenessProto-Oncogene MasProto-Oncogene Protein c-ets-2Proto-Oncogene Proteins c-metRecurrenceHepatocyte Growth FactorMAS1 protein, humanProto-Oncogene MasProto-Oncogene Protein c-ets-2Proto-Oncogene Proteins c-met

Identifiers

PMID23659968
PMCPMC3846434
OpenAlexW1992137695

What OpenQuestion holds

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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.