Evidence map›Paper›PMID 31768389›Full record

ArticleInflammatory intestinal diseases2019

Loss of PTPN23 Promotes Proliferation and Epithelial-to-Mesenchymal Transition in Human Intestinal Cancer Cells.

Lisa van der Lely, Janine Häfliger, Ana Montalban-Arques, Katharina Bäbler, Marlene Schwarzfischer, Max Sabev, Claudia Gottier, Silvia Lang, Michael Scharl, Marianne R Spalinger

Open access · goldAbstract read
In one paragraph

Article in Inflammatory intestinal diseases, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.3field-weighted citation impact, top 43% 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

10 citing papers in PubMed, 11 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

10 authors at 2 institutions in 1 country.

Lisa van der LelyDepartment of Gastroenterology and Hepatology, University Hospital Zurich, and University of Zurich, Zurich, Switzerland.
Janine HäfligerDepartment of Gastroenterology and Hepatology, University Hospital Zurich, and University of Zurich, Zurich, Switzerland.
Ana Montalban-ArquesDepartment of Gastroenterology and Hepatology, University Hospital Zurich, and University of Zurich, Zurich, Switzerland.
Katharina BäblerDepartment of Gastroenterology and Hepatology, University Hospital Zurich, and University of Zurich, Zurich, Switzerland.
Marlene SchwarzfischerDepartment of Gastroenterology and Hepatology, University Hospital Zurich, and University of Zurich, Zurich, Switzerland.
Max SabevDepartment of Gastroenterology and Hepatology, University Hospital Zurich, and University of Zurich, Zurich, Switzerland.
Claudia GottierDepartment of Gastroenterology and Hepatology, University Hospital Zurich, and University of Zurich, Zurich, Switzerland.
Silvia LangDepartment of Gastroenterology and Hepatology, University Hospital Zurich, and University of Zurich, Zurich, Switzerland.
Michael ScharlDepartment of Gastroenterology and Hepatology, University Hospital Zurich, and University of Zurich, Zurich, Switzerland.
Marianne R SpalingerDepartment of Gastroenterology and Hepatology, University Hospital Zurich, and University of Zurich, Zurich, Switzerland.
University Hospital of Zurich · CHUniversity of Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

objectivesProtein tyrosine phosphatase nonreceptor type 23 (PTPN23) has recently been associated with several human epithelial cancers via regulation of growth factor signaling. Colorectal carcinoma (CRC) is a leading cause for cancer-related death worldwide and is associated with aberrant epidermal (EGF) and vascular endothelial growth factor signaling. Here, we investigated whether PTPN23 might play a role in CRC.

methodsExpression of PTPN23 was analyzed in CRC tissue by immunohistochemistry. PTPN23 was silenced in HT-29 cells to address the role of PTPN23 in EGF signaling, gene expression, and cell migration.

resultsPTPN23 silencing in HT-29 and Caco-2 intestinal epithelial cancer cells significantly enhanced activation of pro-oncogenic signaling molecules and genes promoting epithelial-to-mesenchymal transition (EMT) upon EGF treatment, while genes encoding tight junction proteins were significantly reduced.

conclusionsOur data clearly indicate that loss of PTPN23 is associated with increased activation of pro-oncogenic signaling pathways and an enhanced ability of human intestinal cancer cells to undergo EMT. Taken together, these findings show that PTPN23 acts as a tumor suppressor gene in CRC.

Indexed as

Colorectal cancerEGF receptorEpithelial-to-mesenchymal transitionGrowth factor signalingProtein tyrosine phosphatase

Identifiers

PMID31768389
PMCPMC6873011
OpenAlexW2973557703

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Registered trials

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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.