Evidence map›Paper›PMID 26175151›Full record

ArticleThe Journal of biological chemistry2015

Lysophosphatidic Acid Initiates Epithelial to Mesenchymal Transition and Induces β-Catenin-mediated Transcription in Epithelial Ovarian Carcinoma.

Rebecca J Burkhalter, Suzanne D Westfall, Yueying Liu, M Sharon Stack

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

42 citing papers in PubMed, 55 citations in OpenAlex.

  1. Review
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  6. New Target(s) for RNF43 Regulation: Implications for Therapeutic Strategies.International journal of molecular sciences · 2024
    Review
  7. Protein kinase D1 - A targetable mediator of pancreatic cancer development.Biochimica et biophysica acta. Molecular cell research · 2024
    Review
  8. Article
  9. Review
  10. The Role of EMT-Related lncRNAs in Ovarian Cancer.International journal of molecular sciences · 2023
    Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
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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

4 authors at 3 institutions in 1 country.

Rebecca J BurkhalterFrom the Departments of Medical Pharmacology and Physiology and the Harper Cancer Research Institute.
Suzanne D WestfallPathology and Anatomical Sciences, University of Missouri, Columbia, Missouri 65212 and.
Yueying Liuthe Harper Cancer Research Institute, Department of Chemistry and Biochemistry, University of Notre Dame, South Bend, Indiana 46617.
M Sharon Stackthe Harper Cancer Research Institute, Department of Chemistry and Biochemistry, University of Notre Dame, South Bend, Indiana 46617 sstack@nd.edu.
University of Notre Dame · USCancer Research Institute · USUniversity of Missouri · US

Funding

Receptor Cross-Talk in Early Metastatic DisseminationR01CA109545 · NCI · UNIVERSITY OF NOTRE DAME · PI STACK, MARY SHARON · 2006 to 2022
$4.3M
REGULATION OF OVARIAN CARCINOMA PROTEINASESR01CA086984 · NCI · UNIVERSITY OF NOTRE DAME · PI STACK, MARY SHARON · 2000 to 2014
$3.8M
NCI NIH HHS CA086984-11S1NCI NIH HHS R01 CA086984NCI NIH HHS R01 CA109545
6 · The paper itself

Abstract

During tumor progression, epithelial ovarian cancer (EOC) cells undergo epithelial-to-mesenchymal transition (EMT), which influences metastatic success. Mutation-dependent activation of Wnt/β-catenin signaling has been implicated in gain of mesenchymal phenotype and loss of differentiation in several solid tumors; however, similar mutations are rare in most EOC histotypes. Nevertheless, evidence for activated Wnt/β-catenin signaling in EOC has been reported, and immunohistochemical analysis of human EOC tumors demonstrates nuclear staining in all histotypes. This study addresses the hypothesis that the bioactive lipid lysophosphatidic acid (LPA), prevalent in the EOC microenvironment, functions to regulate EMT in EOC. Our results demonstrate that LPA induces loss of junctional β-catenin, stimulates clustering of β1 integrins, and enhances the conformationally active population of surface β1 integrins. Furthermore, LPA treatment initiates nuclear translocation of β-catenin and transcriptional activation of Wnt/β-catenin target genes resulting in gain of mesenchymal marker expression. Together these data suggest that LPA initiates EMT in ovarian tumors through β1-integrin-dependent activation of Wnt/β-catenin signaling, providing a novel mechanism for mutation-independent activation of this pathway in EOC progression.

Indexed as

Active Transport, Cell Nucleusbeta CateninBlotting, WesternCadherinsCarcinoma, Ovarian EpithelialCell Line, TumorEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHumansIntegrin beta1LysophospholipidsMicroscopy, FluorescenceNeoplasms, Glandular and EpithelialOvarian NeoplasmsProtein Bindingbeta CateninCadherinsIntegrin beta1lysophosphatidic acidLysophospholipidsProto-Oncogene ProteinsReceptors, Lysophosphatidic AcidTCF Transcription FactorsVimentinWnt-5a ProteinWNT5A protein, humanWnt ProteinsintegrinLPAlysophospholipidovarian cancerWnt signalingβ-catenin (β-catenin)

Identifiers

PMID26175151
PMCPMC4571965
OpenAlexW2122069948

What OpenQuestion holds

Textmetadata
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.