Evidence map›Paper›PMID 27452517›Full record

ArticleOncogene2017

PIPKIγ and talin couple phosphoinositide and adhesion signaling to control the epithelial to mesenchymal transition.

N Thapa, X Tan, S Choi, T Wise, R A Anderson

Abstract read
In one paragraph

Article in Oncogene, 2017. 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
–field-weighted citation impact
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.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Multi-Pathway Study for Oxaliplatin Resistance Reduction.Current issues in molecular biology · 2025
    Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. PIPKIJournal of immunology research · 2019
    Article
  17. Review
  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.

N ThapaMolecular and Cellular Pharmacology Program, University of Wisconsin-Madison, School of Medicine and Public Health, Madison, WI, USA.
X TanMolecular and Cellular Pharmacology Program, University of Wisconsin-Madison, School of Medicine and Public Health, Madison, WI, USA.ORCID 0000-0003-3300-2240
S ChoiMolecular and Cellular Pharmacology Program, University of Wisconsin-Madison, School of Medicine and Public Health, Madison, WI, USA.
T WiseMolecular and Cellular Pharmacology Program, University of Wisconsin-Madison, School of Medicine and Public Health, Madison, WI, USA.
R A AndersonMolecular and Cellular Pharmacology Program, University of Wisconsin-Madison, School of Medicine and Public Health, Madison, WI, USA.

Funding

Targeting of Phosphoinositide Signaling in Migration, Invasion and MetastasisR01GM057549 · NIGMS · UNIVERSITY OF WISCONSIN-MADISON · PI ANDERSON, RICHARD A. · 1998 to 2019
$5.7M
Phosphoinositide Signaling in the Cytosol and NucleusR35GM134955 · NIGMS · UNIVERSITY OF WISCONSIN-MADISON · PI Richard A. Anderson · 2020 to 2026
$5.0M
PI Signaling Role in Epithelial/Mesenchymal TransitionR01CA104708 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI ANDERSON, RICHARD A. · 2004 to 2014
$2.9M
NCI NIH HHS R01 CA104708NIGMS NIH HHS R01 GM057549NIGMS NIH HHS R35 GM134955
6 · The paper itself

Abstract

Epithelial cells acquire migratory/invasive and stemness traits upon conversion to the mesenchymal phenotype. The expression of E-cadherin is a key to this transition; yet precise understanding of the pathways involved in integrating E-cadherin loss to the gain of mesenchymal traits remains poorly understood. Here, we show that phosphoinositide-generating enzyme, PIPKIγ, expression is upregulated upon epithelial-mesenchymal transition (EMT) and together with the cytoskeletal protein talin assemble into a signaling complex upon E-cadherin loss. PIPKIγ and talin together control the adhesion and phosphoinositide signaling that regulates conversion to the mesenchymal phenotypes. PIPKIγ and talin regulate the stability of E-cadherin transcriptional repressors, snail and slug, induced by transforming growth factor-β1 or extracellular matrix protein. Loss of PIPKIγ or talin or their interaction impaired EMT and the acquisition of cell motility and stemness. This demonstrates a mechanism where a phosphoinositide-generating enzyme PIPKIγ couples with a cytoskeletal protein talin to control the acquisition of mesenchymal phenotypes.

Indexed as

Cell AdhesionEpithelial-Mesenchymal TransitionAnimalsApoptosisCadherinsCell MovementCell ProliferationCells, CulturedCell Transformation, NeoplasticFemaleGene Expression Regulation, NeoplasticMammary Glands, AnimalMicePhosphatidylinositolsPhosphotransferases (Alcohol Group Acceptor)Signal Transduction1-phosphatidylinositol-4-phosphate 5-kinaseCadherinsPhosphatidylinositolsPhosphotransferases (Alcohol Group Acceptor)TalinTln1 protein, mouseTransforming Growth Factor beta1

Identifiers

PMID27452517
PMCPMC6344042

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.