Evidence map›Paper›PMID 23328666›Full record

ArticleCell death & disease2013

The decreased metastatic potential of rhabdomyosarcoma cells obtained through MET receptor downregulation and the induction of differentiation.

K Miekus, E Lukasiewicz, D Jarocha, M Sekula, G Drabik, M Majka

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

25 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Rhabdomyosarcoma.Nature reviews. Disease primers · 2019
    Review
  14. Review
  15. Article
  16. c-MET expression potentially contributes to the poor prognosis of rhabdomyosarcoma.International journal of clinical and experimental pathology · 2018
    Article
  17. Article
  18. Article
  19. Article
  20. 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 1 institution in 1 country.

K MiekusDepartment of Transplantation, Polish-American Institute of Pediatrics, Jagiellonian University School of Medicine, Cracow, Poland.
E Lukasiewicz
D Jarocha
M Sekula
G Drabik
M Majka
Jagiellonian University · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rhabdomyosarcoma (RMS) is the most common type of pediatric soft tissue sarcoma. The MET receptor has an important role in the biology of RMS, and its overexpression and hyperactivation correlate with the metastatic ability of RMS. Consequently, interfering with MET expression or functionality may constitute a sound strategy for reducing the progression and metastatic potential of RMS. Our study reveals that downregulation of the MET receptor leads to changes in the morphology of ARMS cell in vivo. Tumors acquire a spindle shape that is characteristic of muscle fibers. Inhibition of MET expression or function leads to (i) a decreased expression of the early myogenic marker MyoD, (ii) a decreased ability of ARMS cells to metastasize to bone marrow cavities, (iii) downregulation of CXCR4 receptor expression and (iv) a decreased migration of MET-depleted cells towards gradients of HGF and SDF-1. Finally, we demonstrate that in vitro differentiation of alveolar RMS cells decreases their metastatic behavior by reducing both the expression of the MET and CXCR4 receptors and their migratory response to HGF and SDF-1. These findings suggest that blockers of MET receptor function and inducers of RMS cells differentiation may be clinically useful for reducing the aggressiveness and metastatic potential of RMS and may have significant implications for its treatment.

Indexed as

AnimalsBone Marrow NeoplasmsCell DifferentiationCell Line, TumorCell MovementChemokine CXCL12Down-RegulationHepatocyte Growth FactorHumansMiceMice, Inbred NODMice, SCIDMitogen-Activated Protein Kinase KinasesMyoD ProteinPhosphorylationProto-Oncogene Proteins c-aktChemokine CXCL12CXCL12 protein, humanHepatocyte Growth FactorMET protein, humanMitogen-Activated Protein Kinase KinasesMyoD ProteinProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-metReceptors, CXCR4RNA, Small Interfering

Identifiers

PMID23328666
PMCPMC3563987
OpenAlexW2046256823

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.