Evidence map›Paper›PMID 30863185›Full record

ArticleCancer management and research2019

E3 ubiquitin ligase Smurf2: a prognostic factor in microsatellite stable colorectal cancer.

Fee Klupp, Christina Giese, Niels Halama, Clemens Franz, Felix Lasitschka, Arne Warth, Thomas Schmidt, Matthias Kloor, Alexis Ulrich, Martin Schneider

Open access · goldAbstract read
In one paragraph

Article in Cancer management and research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

17 citing papers in PubMed, 22 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.

Fee KluppDepartment of General, Visceral and Transplantation Surgery, University of Heidelberg, Heidelberg 69120, Germany, martin.schneider@med.uni-heidelberg.de.
Christina GieseDepartment of General, Visceral and Transplantation Surgery, University of Heidelberg, Heidelberg 69120, Germany, martin.schneider@med.uni-heidelberg.de.
Niels HalamaNational Center for Tumor Diseases, Medical Oncology and Internal Medicine VI, Tissue Imaging and Analysis Center, Bioquant, University of Heidelberg, Heidelberg 69120, Germany.
Clemens FranzDepartment of General, Visceral and Transplantation Surgery, University of Heidelberg, Heidelberg 69120, Germany, martin.schneider@med.uni-heidelberg.de.
Felix LasitschkaInstitute of Pathology, University of Heidelberg, Heidelberg 69120, Germany.
Arne WarthInstitute of Pathology, University of Heidelberg, Heidelberg 69120, Germany.
Thomas SchmidtDepartment of General, Visceral and Transplantation Surgery, University of Heidelberg, Heidelberg 69120, Germany, martin.schneider@med.uni-heidelberg.de.
Matthias KloorDepartment of Applied Tumor Biology, German Cancer Research Center, Heidelberg 69120, Germany.
Alexis UlrichDepartment of General, Visceral and Transplantation Surgery, University of Heidelberg, Heidelberg 69120, Germany, martin.schneider@med.uni-heidelberg.de.
Martin SchneiderDepartment of General, Visceral and Transplantation Surgery, University of Heidelberg, Heidelberg 69120, Germany, martin.schneider@med.uni-heidelberg.de.
Heidelberg University · DEGerman Cancer Research Center · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeSmurf2 is a member of the homologous to E6-AP carboxyl terminus family of E3 ubiquitin ligases. Changes in their expression pattern are known to contribute to tumorigenesis. Smurf2 plays a decisive role in cell differentiation, proliferation, and migration and exhibits a dual role in cancer - functioning as both oncogene and tumor suppressor. Dysregulation of Smurf2 in different cancer types has been described, besides colorectal cancer (CRC). We therefore examined the expression and oncogenic potential of Smurf2 in human CRC patients. MATERIALS AND

methodsExpression levels of Smurf2 were analyzed via qRT-PCR in CRC specimens and healthy mucosa from 98 patients who had undergone surgery due to CRC. Spatial expression of Smurf2 was additionally studied by immunohistochemistry. siRNA-mediated knockdown of Smurf2 was applied for migration and invasion assays in DLD-1 and SW-480 cells.

resultsSmurf2 was significantly overexpressed in CRC tissue compared to corresponding healthy colon mucosa. Smurf2 expression levels differed significantly between microsatellite instable (MSI) and microsatellite stable (MSS) CRC. In patients suffering from MSS CRC, high tumoral expression of Smurf2 was significantly associated with impaired overall survival. Consistently, in vitro analysis revealed that knockdown of Smurf2 reduced the invasive and migratory potential of MSS CRC cells.

conclusionSmurf2 expression is upregulated in CRC specimens and affects survival dependent on patients' MSI status. Moreover, Smurf2 supports cancer cell migration and invasion, collectively suggesting an oncogenic function in CRC.

Indexed as

biomarkercolorectal cancerMSS statusprognosisSmurf2

Identifiers

PMID30863185
PMCPMC6391146
OpenAlexW2918039826

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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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.