Evidence map›Paper›PMID 26384300›Full record

ArticleOncotarget2015

Constitutive activation of MET signaling impairs myogenic differentiation of rhabdomyosarcoma and promotes its development and progression.

Klaudia Skrzypek, Anna Kusienicka, Barbara Szewczyk, Tomasz Adamus, Ewa Lukasiewicz, Katarzyna Miekus, Marcin Majka

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

21 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
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  7. Antibacterial Therapy by AgInternational journal of molecular sciences · 2021
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  13. miRNA signatures in childhood sarcomas and their clinical implications.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2019
    Review
  14. Review
  15. Rhabdomyosarcoma.Nature reviews. Disease primers · 2019
    Review
  16. Article
  17. Article
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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 1 institution in 1 country.

Klaudia SkrzypekDepartment of Transplantation, Polish-American Institute of Pediatrics, Jagiellonian University Medical College, 30-663 Krakow, Poland.
Anna KusienickaDepartment of Transplantation, Polish-American Institute of Pediatrics, Jagiellonian University Medical College, 30-663 Krakow, Poland.
Barbara SzewczykDepartment of Transplantation, Polish-American Institute of Pediatrics, Jagiellonian University Medical College, 30-663 Krakow, Poland.
Tomasz AdamusDepartment of Transplantation, Polish-American Institute of Pediatrics, Jagiellonian University Medical College, 30-663 Krakow, Poland.
Ewa LukasiewiczDepartment of Transplantation, Polish-American Institute of Pediatrics, Jagiellonian University Medical College, 30-663 Krakow, Poland.
Katarzyna MiekusDepartment of General Biochemistry, Faculty of Biochemistry, Biophysics and Biotechnology, Jagiellonian University, 30-387 Krakow, Poland.
Marcin MajkaDepartment of Transplantation, Polish-American Institute of Pediatrics, Jagiellonian University Medical College, 30-663 Krakow, Poland.
Jagiellonian University · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rhabdomyosarcoma (RMS) is a soft tissue sarcoma, which may originate from impaired differentiation of mesenchymal stem cells (MSC). Expression of MET receptor is elevated in alveolar RMS subtype (ARMS) which is associated with worse prognosis, compared to embryonal RMS (ERMS). Forced differentiation of ARMS cells diminishes MET level and, as shown previously, MET silencing induces differentiation of ARMS. In ERMS cells introduction of TPR-MET oncogene leads to an uncontrolled overstimulation of the MET receptor downstream signaling pathways. In vivo, tumors formed by those cells in NOD-SCID mice display inhibited differentiation, enhanced proliferation, diminished apoptosis and increased infiltration of neutrophils. Consequently, tumors grow significantly faster and they display enhanced ability to metastasize to lungs and to vascularize due to elevated VEGF, MMP9 and miR-378 expression. In vitro, TPR-MET ERMS cells display enhanced migration, chemotaxis and invasion toward HGF and SDF-1. Introduction of TPR-MET into MSC increases survival and may induce expression of early myogenic factors depending on the genetic background, and it blocks terminal differentiation of skeletal myoblasts. To conclude, our results suggest that activation of MET signaling may cause defects in myogenic differentiation leading to rhabdomyosarcoma development and progression.

Indexed as

Cell DifferentiationCell MovementCell ProliferationNeovascularization, PathologicAnimalsApoptosisBlotting, WesternCells, CulturedCell Transformation, NeoplasticFlow CytometryHumansHuman Umbilical Vein Endothelial CellsMiceMice, Inbred NODMice, SCIDMyoblastsMET protein, humanProto-Oncogene Proteins c-metRNA, Messengerdifferentiationmesenchymal stem cells (MSC)METmetastasisrhabdomyosarcoma (RMS)

Identifiers

PMID26384300
PMCPMC4741613
OpenAlexW2144260663

What OpenQuestion holds

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LicenceCC BY
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.