Evidence map›Paper›PMID 28054314›Full record

ArticlePathology oncology research : POR2017

Turning back the Wheel: Inducing Mesenchymal to Epithelial Transition via Wilms Tumor 1 Knockdown in Human Mesothelioma Cell Lines to Influence Proliferation, Invasiveness, and Chemotaxis.

Till Plönes, Mitja Fischer, Kerstin Höhne, Hiromi Sato, Joachim Müller-Quernheim, Gernot Zissel

Abstract read
PubMed Publisher
In one paragraph

Article in Pathology oncology research : POR, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.7field-weighted citation impact, top 32% 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

8 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Genomics and Functional Genomics of Malignant Pleural Mesothelioma.International journal of molecular sciences · 2020
    Review
  6. Article
  7. Article
  8. 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 4 institutions in 2 countries.

Till PlönesDepartment of Thoracic Surgery and Thoracic Endoscopy, Ruhrlandklinik, West German Lung Center, University Hospital Essen, University Duisburg-Essen, Essen, Germany. Till_ploenes@gmx.de.
Mitja FischerDepartment of Pneumology, Center for Medicine, Medical Center University of Freiburg, Freiburg, Germany.
Kerstin HöhneDepartment of Pneumology, Center for Medicine, Medical Center University of Freiburg, Freiburg, Germany.
Hiromi SatoGraduate School of Pharmaceutical Sciences, Department of Clinical Pharmacology & Pharmacometrics, Chiba University, 1-8-1 Inohana, Chuou-ku, Chiba, 260-8675, Japan.
Joachim Müller-QuernheimDepartment of Pneumology, Center for Medicine, Medical Center University of Freiburg, Freiburg, Germany.
Gernot ZisselDepartment of Pneumology, Center for Medicine, Medical Center University of Freiburg, Freiburg, Germany.
University Medical Center Freiburg · DEUniversity of Freiburg · DEChiba University · JPRuhrlandklinik · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Malignant pleural mesothelioma (MPM) is a highly aggressive tumor that arises from the surface of the pleura and is associated with a history of asbestos exposure. The tumor is characterized by a strong local invasiveness and a poor response to any single modality therapy. Therefore clinical outcome of patients with MPM is poor and median survival time of untreated patients with MPM is 7 months from initial diagnosis. The Wilms Tumor Protein 1 (WT1) is a transcription factor which is highly expressed by MPM and is involved in cellular development and survival. We evaluated the role of WT1 in two human MPM cell lines (MSTO and H2052) expressing high levels of WT1. We performed a knockdown of WT1 using siRNA. Knockdown of WT1 was confirmed by Westernblotting. After knockdown of WT1 we investigated the effect on proliferation, chemoresistance, chemotaxis and migration. We could demonstrate that knockdown of WT1 suppresses chemoresistance in both cell lines compared with control (scrambled siRNA). Additionally, WT1 knockdown reduces proliferation, chemotaxis and invasiveness of mesothelioma cell lines. WT1 reduces malignancy of malignant mesothelioma cell lines and might be a new molecular target in mesothelioma therapy. Further investigations are needed to discover the mechanisms of chemoresistance depending on WT1.

Indexed as

Cell Line, TumorCell ProliferationChemotaxisDrug Resistance, NeoplasmGene Knockdown TechniquesHumansLung NeoplasmsMesotheliomaMesothelioma, MalignantNeoplasm InvasivenessPleural NeoplasmsWT1 ProteinsWT1 protein, humanWT1 ProteinsAsbestosCancerChemoresistanceCisplatinDecorticationDrugEMTEpigeneticsEpithelial to mesenchymal transitionEPPMetP/DPleuralPleuropneumonectomyStem cellsWilms tumor

Identifiers

PMID28054314
OpenAlexW2570145329

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.