Evidence map›Paper›PMID 25578398›Full record

ArticleBiochimica et biophysica acta2015

The APC tumor suppressor is required for epithelial cell polarization and three-dimensional morphogenesis.

Alyssa C Lesko, Kathleen H Goss, Frank F Yang, Adam Schwertner, Imge Hulur, Kenan Onel, Jenifer R Prosperi

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

Article in Biochimica et biophysica acta, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.9field-weighted citation impact, top 24% 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

11 citing papers in PubMed, 27 citations in OpenAlex.

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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

7 authors at 2 institutions in 1 country.

Alyssa C LeskoDepartment of Biological Sciences and Harper Cancer Research Institute, University of Notre Dame, Notre Dame, IN 46556, USA.
Kathleen H GossUniversity of Chicago Medicine Comprehensive Cancer Center, Chicago, IL 60637, USA.
Frank F YangDepartment of Surgery, University of Chicago, Chicago, IL 60637, USA.
Adam SchwertnerDepartment of Surgery, University of Chicago, Chicago, IL 60637, USA.
Imge HulurDepartment of Pediatrics, University of Chicago, Chicago, IL 60637, USA.
Kenan OnelDepartment of Pediatrics, University of Chicago, Chicago, IL 60637, USA.
Jenifer R ProsperiDepartment of Biochemistry and Molecular Biology, Indiana University School of Medicine - South Bend, South Bend, IN 46617, USA; Department of Biological Sciences and Harper Cancer Research Institute, University of Notre Dame, Notre Dame, IN 46556, USA. Electronic address: jrprospe@iupui.edu.
University of Chicago · USUniversity of Notre Dame · US

Funding

ULTRASTRUCTURE AND CYTOMORPHOLOGY COREP30DK042086 · NIDDK · UNIVERSITY OF CHICAGO · PI LIU, CAMBRIAN YANGSHAO · 1990 to 2025
$29.8M
Re-Engineering Translational Research at the University of ChicagoUL1TR000430 · NCATS · UNIVERSITY OF CHICAGO · PI SOLWAY, JULIAN · 2012 to 2016
$20.2M
NCATS NIH HHS UL1 TR000430NIDDK NIH HHS P30 DK042086NIDDK NIH HHS P30DK42086
6 · The paper itself

Abstract

The Adenomatous Polyposis Coli (APC) tumor suppressor has been previously implicated in the control of apical-basal polarity; yet, the consequence of APC loss-of-function in epithelial polarization and morphogenesis has not been characterized. To test the hypothesis that APC is required for the establishment of normal epithelial polarity and morphogenesis programs, we generated APC-knockdown epithelial cell lines. APC depletion resulted in loss of polarity and multi-layering on permeable supports, and enlarged, filled spheroids with disrupted polarity in 3D culture. Importantly, these effects of APC knockdown were independent of Wnt/β-catenin signaling, but were rescued with either full-length or a carboxy (c)-terminal segment of APC. Moreover, we identified a gene expression signature associated with APC knockdown that points to several candidates known to regulate cell-cell and cell-matrix communication. Analysis of epithelial tissues from mice and humans carrying heterozygous APC mutations further supports the importance of APC as a regulator of epithelial behavior and tissue architecture. These data also suggest that the initiation of epithelial-derived tumors as a result of APC mutation or gene silencing may be driven by loss of polarity and dysmorphogenesis.

Indexed as

Adenomatous Polyposis Coli ProteinAnimalsCell Culture TechniquesCell PolarityCells, CulturedDogsEpithelial CellsGene Knockdown TechniquesGenes, Tumor SuppressorHEK293 CellsHumansMiceMorphogenesisMutationAdenomatous Polyposis Coli ProteinAPC protein, humanAdenomatous Polyposis ColiEpithelial polarityMadin–Darby Canine Kidney

Identifiers

PMID25578398
PMCPMC4327896
OpenAlexW2065244533

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.