Evidence map›Paper›PMID 24727894›Full record

ArticleOncogene2015

δ-Catenin, a Wnt/β-catenin modulator, reveals inducible mutagenesis promoting cancer cell survival adaptation and metabolic reprogramming.

J Nopparat, J Zhang, J-P Lu, Y-H Chen, D Zheng, P D Neufer, J M Fan, H Hong, C Boykin, Q Lu

Open access · bronzeAbstract read
In one paragraph

Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

27 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Roles and regulation of δ-catenin in tumorigenesis and neuronal diseases.Frontiers in cell and developmental biology · 2025
    Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Delta-Catenin as a Modulator of Rho GTPases in Neurons.Frontiers in cellular neuroscience · 2022
    Review
  17. The Hypoxia-Long Noncoding RNA Interaction in Solid Cancers.International journal of molecular sciences · 2021
    Review
  18. Article
  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 2 countries.

J NopparatDepartment of Anatomy and Cell Biology, The Brody School of Medicine, East Carolina University, Greenville, NC, USA.
J ZhangDepartment of Anatomy and Cell Biology, The Brody School of Medicine, East Carolina University, Greenville, NC, USA.
J-P LuCollege of Life Sciences, Zhejiang University, Hangzhou, China.
Y-H Chen1] Department of Anatomy and Cell Biology, The Brody School of Medicine, East Carolina University, Greenville, NC, USA [2] Leo Jenkins Cancer Center, The Brody School of Medicine, East Carolina University, Greenville, NC, USA [3] Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, NC, USA.
D Zheng1] Department of Kinesiology, East Carolina University, Greenville, NC, USA [2] East Carolina Diabetes and Obesity Institute, East Carolina University, Greenville, NC, USA.
P D Neufer1] Department of Kinesiology, East Carolina University, Greenville, NC, USA [2] East Carolina Diabetes and Obesity Institute, East Carolina University, Greenville, NC, USA [3] Department of Physiology, The Brody School of Medicine, East Carolina University, Greenville, NC, USA.
J M FanDepartment of Anatomy and Cell Biology, The Brody School of Medicine, East Carolina University, Greenville, NC, USA.
H HongDepartment of Pathology and Laboratory Medicine, The Brody School of Medicine, East Carolina University, Greenville, NC, USA.
C BoykinDepartment of Anatomy and Cell Biology, The Brody School of Medicine, East Carolina University, Greenville, NC, USA.
Q Lu1] Department of Anatomy and Cell Biology, The Brody School of Medicine, East Carolina University, Greenville, NC, USA [2] Leo Jenkins Cancer Center, The Brody School of Medicine, East Carolina University, Greenville, NC, USA [3] Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, NC, USA.
East Carolina University · USUniversity of North Carolina at Chapel Hill · USZhejiang University · CN

Funding

Linking Mitochondrial Bioenergetics to Muscle Insulin SensitivityR01DK074825 · NIDDK · EAST CAROLINA UNIVERSITY · PI NEUFER, P DARRELL · 2009 to 2013
$1.6M
Redox Biology and Muscle Insulin SensitivityR01DK096907 · NIDDK · EAST CAROLINA UNIVERSITY · PI NEUFER, P DARRELL · 2012 to 2015
$1.4M
Mitochondrial Bioenergetics and Etiology of Insulin ResistanceR01DK073488 · NIDDK · EAST CAROLINA UNIVERSITY · PI NEUFER, P DARRELL · 2007 to 2010
$1.2M
delta-Catenin and Cell-Cell Adhesion in Prostate CancerR01CA111891 · NCI · EAST CAROLINA UNIVERSITY · PI LU, QUN · 2006 to 2010
$759k
Rho GTPases and Neuroprotection Model in Cancer TherapyR15CA165202 · NCI · EAST CAROLINA UNIVERSITY · PI LU, QUN · 2012 to 2014
$500k
Roles of Claudin-7 in Lung CancerR03ES016888 · NIEHS · EAST CAROLINA UNIVERSITY · PI CHEN, YAN-HUA · 2008 to 2009
$143k
NCI NIH HHS CA111891NCI NIH HHS CA165202NCI NIH HHS R01 CA111891NCI NIH HHS R15 CA165202NIDDK NIH HHS DK073488NIDDK NIH HHS DK074825NIDDK NIH HHS R01 DK073488NIDDK NIH HHS R01 DK074825NIDDK NIH HHS R01 DK096907NIEHS NIH HHS ES016888NIEHS NIH HHS R03 ES016888
6 · The paper itself

Abstract

Mutations of Wnt/β-catenin signaling pathway has essential roles in development and cancer. Although β-catenin and adenomatous polyposis coli (APC) gene mutations are well established and are known to drive tumorigenesis, discoveries of mutations in other components of the pathway lagged, which hinders the understanding of cancer mechanisms. Here we report that δ-catenin (gene designation: CTNND2), a primarily neural member of the β-catenin superfamily that promotes canonical Wnt/β-catenin/LEF-1-mediated transcription, displays exonic mutations in human prostate cancer and promotes cancer cell survival adaptation and metabolic reprogramming. When overexpressed in cells derived from prostate tumor xenografts, δ-catenin gene invariably gives rise to mutations, leading to sequence disruptions predicting functional alterations. Ectopic δ-catenin gene integrating into host chromosomes is locus nonselective. δ-Catenin mutations promote tumor development in mouse prostate with probasin promoter (ARR2PB)-driven, prostate-specific expression of Myc oncogene, whereas mutant cells empower survival advantage upon overgrowth and glucose deprivation. Reprogramming energy utilization accompanies the downregulation of glucose transporter-1 and poly (ADP-ribose) polymerase cleavage while preserving tumor type 2 pyruvate kinase expression. δ-Catenin mutations increase β-catenin translocation to the nucleus and hypoxia-inducible factor 1α (HIF-1α) expression. Therefore, introducing δ-catenin mutations is an important milestone in prostate cancer metabolic adaptation by modulating β-catenin and HIF-1α signaling under glucose shortage to amplify its tumor-promoting potential.

Indexed as

Animalsbeta CateninCateninsCell Line, TumorCell Transformation, NeoplasticDelta CateninEnergy MetabolismGlucoseHumansMaleMiceMutationNeoplasm TransplantationProstatic NeoplasmsWnt Signaling Pathwaybeta CateninCateninsCTNNB1 protein, humanCTNNB1 protein, mouseDelta CateninGlucose

Identifiers

PMID24727894
PMCPMC4197123
OpenAlexW2055562299

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.