Evidence map›Paper›PMID 24037530›Full record

ArticleOncogene2014

miR-93-directed downregulation of DAB2 defines a novel oncogenic pathway in lung cancer.

L Du, Z Zhao, X Ma, T-H Hsiao, Y Chen, E Young, M Suraokar, I Wistuba, J D Minna, A Pertsemlidis

Open access · bronzeAbstract read
In one paragraph

Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

56 citing papers in PubMed, 82 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. MiRNA-93: a novel signature in human disorders and drug resistance.Cell communication and signaling : CCS · 2023
    Review
  5. Article
  6. Disabled-2 (International journal of molecular sciences · 2022
    Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. [MicroRNA and Lung Cancer: A Mini Review].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2018
    Review
  19. Article
  20. Article
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

10 authors at 3 institutions in 1 country.

L Du1] Greehey Children's Cancer Research Institute, UT Health Science Center at San Antonio, San Antonio, TX, USA [2] Department of Cellular and Structural Biology, UT Health Science Center at San Antonio, San Antonio, TX, USA.
Z ZhaoGreehey Children's Cancer Research Institute, UT Health Science Center at San Antonio, San Antonio, TX, USA.
X MaGreehey Children's Cancer Research Institute, UT Health Science Center at San Antonio, San Antonio, TX, USA.
T-H HsiaoGreehey Children's Cancer Research Institute, UT Health Science Center at San Antonio, San Antonio, TX, USA.
Y Chen1] Greehey Children's Cancer Research Institute, UT Health Science Center at San Antonio, San Antonio, TX, USA [2] Department of Epidemiology & Biostatistics, UT Health Science Center at San Antonio, San Antonio, TX, USA.
E YoungGreehey Children's Cancer Research Institute, UT Health Science Center at San Antonio, San Antonio, TX, USA.
M SuraokarDepartment of Thoracic/Head and Neck Medical Oncology, UT MD Anderson Cancer Center, Houston, TX, USA.
I Wistuba1] Department of Thoracic/Head and Neck Medical Oncology, UT MD Anderson Cancer Center, Houston, TX, USA [2] Department of Translational Molecular Pathology, UT MD Anderson Cancer Center, Houston, TX, USA.
J D MinnaHamon Center for Therapeutic Oncology Research and Departments of Pharmacology and Internal Medicine, UT Southwestern Medical Center at Dallas, Dallas, TX, USA.
A Pertsemlidis1] Greehey Children's Cancer Research Institute, UT Health Science Center at San Antonio, San Antonio, TX, USA [2] Department of Cellular and Structural Biology, UT Health Science Center at San Antonio, San Antonio, TX, USA [3] Department of Pediatrics, UT Health Science Center at San Antonio, San Antonio, TX, USA.
The University of Texas Health Science Center at Houston · USThe University of Texas MD Anderson Cancer Center · USSouthwestern Medical Center

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Fabien Delerue · 1985 to 2026
$290.8M
TISSUE CULTURE---COREP30CA054174 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Robin Jean Leach · 1991 to 2026
$59.1M
UNIVERSITY OF TEXAS--SPORE IN LUNG CANCERP50CA070907 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI HEYMACH, JOHN V., MINNA, JOHN D. · 1996 to 2024
$57.4M
UT Southwestern Medical Center Simmons Comprehensive Cancer CenterP30CA142543 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI MELANIE H. COBB · 2010 to 2026
$53.7M
microRNA regulation of drug sensitivity in non-small cell lung cancerR01CA129632 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI PERTSEMLIDIS, ALEXANDER · 2007 to 2011
$1.6M
NCI NIH HHS P30 CA016672NCI NIH HHS P30 CA054174NCI NIH HHS P30 CA142543NCI NIH HHS P50 CA070907NCI NIH HHS P50 CA70907NCI NIH HHS R01 CA129632
6 · The paper itself

Abstract

The disabled homolog 2 (DAB2) gene was recently identified as a tumor suppressor gene with its expression downregulated in multiple cancer types. The role of DAB2 in lung tumorigenesis, however, is not fully characterized, and the mechanisms of DAB2 dysregulation in lung cancer are not defined. Here we show that low DAB2 levels in lung tumor specimens are significantly correlated with poor patient survival, and that DAB2 overexpression significantly inhibits cell growth in cultured lung cancer cells, indicating its potent tumor suppressor function. We next identify that microRNA miR-93 functions as a potent repressor of DAB2 expression by directly targeting the 3'UTR of the DAB2 mRNA. Using in vitro and in vivo approaches, we demonstrate that miR-93 overexpression has an important role in promoting lung cancer cell growth, and that its oncogenic function is primarily mediated by downregulating DAB2 expression. Our clinical investigations further indicate that high tumor levels of miR-93 are correlated with poor survival of lung cancer patients. The correlations of both low DAB2 and high miR-93 expression levels with poor patient survival strongly support the critical role of the miR-93/DAB2 pathway in determining lung cancer progression.

Indexed as

Gene Expression Regulation, Neoplastic3' Untranslated RegionsAdaptor Proteins, Signal TransducingAnimalsApoptosis Regulatory ProteinsBase SequenceBinding SitesCarcinoma, Non-Small-Cell LungCell Line, TumorCell ProliferationDisease-Free SurvivalFemaleG1 Phase Cell Cycle CheckpointsHumansKaplan-Meier EstimateLung Neoplasms3' Untranslated RegionsAdaptor Proteins, Signal TransducingApoptosis Regulatory ProteinsDAB2 protein, humanMicroRNAsMIRN93 microRNA, humanRNA, MessengerTumor Suppressor Proteins

Identifiers

PMID24037530
PMCPMC4281941
OpenAlexW2092706476

What OpenQuestion holds

Textmetadata
LicenceTDM
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.