Evidence map›Paper›PMID 26477318›Full record

ArticleOncogene2016

N-cadherin functions as a growth suppressor in a model of K-ras-induced PanIN.

Y Su, J Li, C Shi, R H Hruban, G L Radice

Open access · bronzeAbstract 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. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.0field-weighted citation impact, top 22% 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

19 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Signaling pathways and targeted interventions for precancers.Signal transduction and targeted therapy · 2026
    Review
  3. Article
  4. Research in pharmaceutical sciences · 2025
    Article
  5. Article
  6. Proteomics in pancreatic cancer.Biomarker research · 2025
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. 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

5 authors at 3 institutions in 1 country.

Y SuDepartment of Medicine, Center for Translational Medicine, Thomas Jefferson University, Philadelphia, PA, USA.
J LiDepartment of Medicine, Center for Translational Medicine, Thomas Jefferson University, Philadelphia, PA, USA.
C ShiDepartment of Pathology, Microbiology, and Immunology, Vanderbilt University School of Medicine, Nashville, TN, USA.
R H HrubanDepartments of Pathology and Oncology, The Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
G L RadiceDepartment of Medicine, Center for Translational Medicine, Thomas Jefferson University, Philadelphia, PA, USA.
Thomas Jefferson University · USCancer Research Center · USJohns Hopkins Medicine · US

Funding

X-Ray Crystallography and Macromolecular CharacterizationP30CA056036 · NCI · THOMAS JEFFERSON UNIVERSITY · PI DANIEL P SILVER · 1995 to 2026
$94.8M
Tumor Antigens for Individual Signatures and TherapyP50CA062924 · NCI · JOHNS HOPKINS UNIVERSITY · PI LENNON, ANNE MARIE · 1993 to 2022
$54.6M
N-cadherin and Metastatic DisseminationR21CA176097 · NCI · THOMAS JEFFERSON UNIVERSITY · PI RADICE, GLENN LAWRENCE · 2014 to 2015
$371k
NCI NIH HHS P30 CA056036NCI NIH HHS P50 CA062924NCI NIH HHS R21 CA176097
6 · The paper itself

Abstract

Cadherin subtype switching from E-cadherin to N-cadherin is associated with the epithelial-to-mesenchymal transition (EMT), a process required for invasion and dissemination of carcinoma cells. We found that N-cadherin is expressed in human and mouse pancreatic intraepithelial neoplasia (PanIN), suggesting that N-cadherin may also have a role in early-stage pancreatic cancer. To investigate the role of N-cadherin in mouse PanIN (mPanIN), we simultaneously activated oncogenic K-ras(G12D) and deleted the N-cadherin (Cdh2) gene in the murine pancreas. Genetic ablation of N-cadherin (N-cad KO) caused hyperproliferation, accelerated mPanIN progression, and early tumor development in K-ras(G12D) mice. Decreased E-cadherin and redistribution of β-catenin accompanied the loss of N-cadherin in pancreatic ductal epithelial cells (PDEC). Nuclear accumulation of β-catenin and its transcription co-activator Tcf4 led to activation of Wnt/β-catenin target genes. Unexpectedly, loss of N-cadherin in the K-ras(G12D) model resulted in increased mPanIN progression and tumor incidence. These in vivo results demonstrate for the first time that N-cadherin functions as a growth suppressor in the context of oncogenic K-ras.

Indexed as

Animalsbeta CateninCadherinsCell LineCell ProliferationDisease Models, AnimalDisease ProgressionEpithelial-Mesenchymal TransitionHumansImmunoblottingImmunohistochemistryMice, KnockoutMice, TransgenicPancreasPancreatic NeoplasmsPrecancerous Conditionsbeta CateninCadherinsProto-Oncogene Proteins p21(ras)

Identifiers

PMID26477318
PMCPMC4837100
OpenAlexW1958375456

What OpenQuestion holds

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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.