Evidence map›Paper›PMID 26434583›Full record

ArticleOncogene2016

Atypical role of sprouty in colorectal cancer: sprouty repression inhibits epithelial-mesenchymal transition.

Q Zhang, T Wei, K Shim, K Wright, K Xu, H L Palka-Hamblin, A Jurkevich, S Khare

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

24 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
  2. Article
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  4. Review
  5. Article
  6. Article
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  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. MicroRNAs and Apoptosis in Colorectal Cancer.International journal of molecular sciences · 2020
    Review
  14. Loss of Spry1 reduces growth of BRAFCell death & disease · 2020
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 4 institutions in 1 country.

Q ZhangDepartment of Internal Medicine, Section of Gastroenterology and Hepatology, University of Missouri, Columbia, MO, USA.
T WeiDepartment of Internal Medicine, Section of Gastroenterology and Hepatology, University of Missouri, Columbia, MO, USA.
K ShimDepartment of Pediatrics, Medical College of Wisconsin, Milwaukee, WI, USA.
K WrightDepartment of Pediatrics, Medical College of Wisconsin, Milwaukee, WI, USA.
K XuDepartment of Internal Medicine, Section of Gastroenterology and Hepatology, University of Missouri, Columbia, MO, USA.
H L Palka-HamblinDepartment of Biochemistry and Molecular Genetics, University of Illinois at Chicago, Chicago, IL, USA.
A JurkevichMolecular Cytology Core, University of Missouri, Columbia, MO, USA.
S KhareDepartment of Internal Medicine, Section of Gastroenterology and Hepatology, University of Missouri, Columbia, MO, USA.
University of Missouri · USMedical College of Wisconsin · USHarry S. Truman Memorial Veterans' Hospital · USUniversity of Illinois Chicago · US

Funding

Genetic Analysis of the Induction and Morphogenesis of the Inner EarR01DC010387 · NIDCD · MEDICAL COLLEGE OF WISCONSIN · PI SHIM, KATHERINE · 2010 to 2014
$1.8M
Colon Cancer ChemopreventionR03CA150081 · NCI · UNIVERSITY OF MISSOURI-COLUMBIA · PI KHARE, SHARAD · 2010 to 2011
$146k
SPROUTY: PUTATIVE ONCOGENE IN COLORECTAL CANCERI01BX000824 · VA · HARRY S. TRUMAN MEMORIAL VA HOSPITAL · PI KHARE, SHARAD · 2012 to 2025
–
BLRD VA I01 BX000824Intramural VA VA999999NCI NIH HHS R03 CA150081NIDCD NIH HHS R01 DC010387
6 · The paper itself

Abstract

Sprouty (SPRY) appears to act as a tumor suppressor in cancer, whereas we demonstrated that SPRY2 functions as a putative oncogene in colorectal cancer (CRC) (Oncogene, 2010, 29: 5241-5253). We investigated the mechanisms by which SPRY regulates epithelial-mesenchymal transition (EMT) in CRC. SPRY1 and SPRY2 mRNA transcripts were significantly upregulated in human CRC. Suppression of SPRY2 repressed AKT2 and EMT-inducing transcription factors and significantly increased E-cadherin expression. Concurrent downregulation of SPRY1 and SPRY2 also increased E-cadherin and suppressed mesenchymal markers in colon cancer cells. An inverse expression pattern between AKT2 and E-cadherin was established in a human CRC tissue microarray. SPRY2 negatively regulated miR-194-5p that interacts with AKT2 3' untranslated region. Mir-194 mimics increased E-cadherin expression and suppressed cancer cell migration and invasion. By confocal microscopy, we demonstrated redistribution of E-cadherin to plasma membrane in colon cancer cells transfected with miR-194. Spry1(-/-) and Spry2(-/-) double mutant mouse embryonic fibroblasts exhibited decreased cell migration while acquiring several epithelial markers. In CRC, SPRY drive EMT and may serve as a biomarker of poor prognosis.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsAntigens, CDCadherinsColorectal NeoplasmsEpithelial-Mesenchymal TransitionFemaleHumansIntracellular Signaling Peptides and ProteinsMembrane ProteinsMicePhosphoproteinsProtein Serine-Threonine KinasesProto-Oncogene Proteins c-aktTransfectionUp-RegulationAdaptor Proteins, Signal TransducingAKT2 protein, humanAntigens, CDCadherinsCDH1 protein, humanIntracellular Signaling Peptides and ProteinsMembrane ProteinsPhosphoproteinsProtein Serine-Threonine KinasesProto-Oncogene Proteins c-aktSPRY1 protein, humanSpry1 protein, mouseSPRY2 protein, humanSpry2 protein, mouse

Identifiers

PMID26434583
PMCPMC4850112
OpenAlexW2238843374

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.