Evidence map›Paper›PMID 22301110›Full record

ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2012

TNF-α induces upregulation of EGFR expression and signaling in human colonic myofibroblasts.

James Yoo, Citlali Ekaterina Rodriguez Perez, Wenxian Nie, Robert A Edwards, James Sinnett-Smith, Enrique Rozengurt

Abstract read
In one paragraph

Article in American journal of physiology. Gastrointestinal and liver physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

32 citing papers in PubMed, 41 citations in OpenAlex.

  1. Review
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  20. ADAM17 is a Tumor Promoter and Therapeutic Target in Western Diet-associated Colon Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2017
    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

6 authors at 2 institutions in 1 country.

James YooDepartment of Surgery, David Geffen School of Medicine, CURE: Digestive Diseases Research Center and Molecular Biology Institute, University of California, Los Angeles, CA 90095, USA. jayoo@mednet.ucla.edu
Citlali Ekaterina Rodriguez Perez
Wenxian Nie
Robert A Edwards
James Sinnett-Smith
Enrique Rozengurt
Human BioMolecular Research Institute · USUniversity of California, Los Angeles · US

Funding

Pilot and Feasibility ProgramP30DK041301 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ROZENGURT, JUAN ENRIQUE · 1990 to 2019
$18.0M
GASTROINTESTINAL PEPTIDE SIGNALING THROUGH PKC/PKDR01DK055003 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ROZENGURT, JUAN ENRIQUE · 1999 to 2011
$4.9M
GI PEPTIDE SIGNALING THROUGH TYROSINE PHOSPHORYLATIONR01DK056930 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ROZENGURT, JUAN ENRIQUE · 2000 to 2010
$3.0M
Pro-inflammatory Mediator Crosstalk Induces COX-2 in Myofibroblasts via PKC/PKDK08DK085136 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI YOO, JAMES · 2010 to 2014
$759k
Targeting crosstalk between insulin and Gq signaling systems in pancreatic cancerR21CA137292 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ROZENGURT, JUAN ENRIQUE · 2009 to 2010
$373k
NCI NIH HHS R21-CA-137292NIDDK NIH HHS 5K08-DK-085136-02NIDDK NIH HHS K08 DK085136NIDDK NIH HHS P30-DK41301NIDDK NIH HHS R0-1DK-55003NIDDK NIH HHS R01-DK-56930
6 · The paper itself

Abstract

The myofibroblast has recently been identified as an important mediator of tumor necrosis factor-α (TNF-α)-associated colitis and cancer, but the mechanism(s) involved remains incompletely understood. Recent evidence suggests that TNF-α is a central regulator of multiple inflammatory signaling cascades. One important target of TNF-α may be the signaling pathway downstream of the epidermal growth factor receptor (EGFR), which has been associated with many human cancers. Here, we show that long-term exposure of 18Co cells, a model of human colonic myofibroblasts, with TNF-α led to a striking increase in cell surface EGFR expression, an effect that was completely inhibited by cycloheximide. Subsequent EGFR binding by EGF and heparin binding (HB)-EGF was associated with enhanced EGFR tyrosine kinase activity, prolonged ERK activation, and a significant increase in cyclooxygenase-2 (COX-2) expression compared with 18Co cells treated with EGF and HB-EGF alone. TNF-α also increased EGFR expression and signaling in primary myofibroblasts isolated from human colon tissue. TNF-α-induced upregulation of EGFR may be a plausible mechanism to explain the exaggerated cellular responsiveness that characterizes inflammatory bowel disease and that may contribute to a microenvironment that predisposes to colitis-associated cancer through enhanced COX-2 expression.

Indexed as

Blotting, WesternCells, CulturedColonCyclooxygenase 2Enzyme ActivationEpidermal Growth FactorErbB ReceptorsExtracellular Signal-Regulated MAP KinasesHumansImmunoprecipitationMyofibroblastsPhosphorylationProtein BiosynthesisProtein Synthesis InhibitorsQuantum DotsSignal TransductionCyclooxygenase 2EGFR protein, humanEpidermal Growth FactorErbB ReceptorsExtracellular Signal-Regulated MAP KinasesProtein Synthesis InhibitorsTumor Necrosis Factor-alpha

Identifiers

PMID22301110
PMCPMC3355565
OpenAlexW2104747524

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.