Evidence map›Paper›PMID 20123981›Full record

ArticleMolecular and cellular biology2010

Modulation of cellular migration and survival by c-Myc through the downregulation of urokinase (uPA) and uPA receptor.

Daniela Alfano, Giuseppina Votta, Almut Schulze, Julian Downward, Mario Caputi, Maria Patrizia Stoppelli, Ingram Iaccarino

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 20% 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, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.

  1. Pooled it
  2. Review
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  5. Article
  6. Review
  7. Article
  8. Article
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  15. lncRNAs and MYC: An Intricate Relationship.International journal of molecular sciences · 2017
    Review
  16. Article
  17. MINCR is a MYC-induced lncRNA able to modulate MYC's transcriptional network in Burkitt lymphoma cells.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  18. Susceptibility to oral cancers with CD95 and CD95L promoter SNPs may vary with the site and gender.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    Article
  19. 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 5 institutions in 2 countries.

Daniela AlfanoInstitute of Genetics and Biophysics Adriano Buzzati-Traverso, Consiglio Nazionale delle Ricerche (CNR), Via P. Castellino 111, 80131 Naples, Italy.
Giuseppina Votta
Almut Schulze
Julian Downward
Mario Caputi
Maria Patrizia Stoppelli
Ingram Iaccarino
Institute of Genetics and Biophysics · ITCancer Research UK · GBNational Research Council · ITThe Honourable Society of Lincoln's Inn · GBUniversity of Campania "Luigi Vanvitelli" · IT

Funding

Worldwide Cancer Research 05-0416
6 · The paper itself

Abstract

It has been proposed that c-Myc proapoptotic activity accounts for most of its restraint of tumor formation. We established a telomerase-immortalized human epithelial cell line expressing an activatable c-Myc protein. We found that c-Myc activation induces, in addition to increased sensitivity to apoptosis, reductions in cell motility and invasiveness. Transcriptome analysis revealed that urokinase (uPA) and uPA receptor (uPAR) were strongly downregulated by c-Myc. Evidence is provided that the repression of uPA and uPAR may account for most of the antimigratory and proapoptotic activities of c-Myc. c-Myc is known to cooperate with Ras in cellular transformation. We therefore investigated if this cooperation could converge in the control of uPA/uPAR expression. We found that Ras is able to block the effects of c-Myc activation on apoptosis and cellular motility but not on cell invasiveness. Accordingly, the activation of c-Myc in the context of Ras expression had only minor influence on uPAR expression but still had a profound repressive effect on uPA expression. Thus, the differential regulation of uPA and uPAR by c-Myc and Ras correlates with the effects of these two oncoproteins on cell motility, invasiveness, and survival. In conclusion, we have discovered a novel link between c-Myc and uPA/uPAR. We propose that reductions of cell motility and invasiveness could contribute to the inhibition of tumorigenesis by c-Myc and that the regulation of uPA and uPAR expression may be a component of the ability of c-Myc to reduce motility and invasiveness.

Indexed as

ApoptosisCell LineCell MovementCell SurvivalChemokinesCulture Media, ConditionedCyclin-Dependent Kinase Inhibitor p21Down-RegulationEnzyme ActivationEpithelial CellsGene SilencingHumansKruppel-Like Transcription FactorsProto-Oncogene Proteins c-mycras ProteinsReceptors, Urokinase Plasminogen ActivatorChemokinesCulture Media, ConditionedCyclin-Dependent Kinase Inhibitor p21Kruppel-Like Transcription FactorsProto-Oncogene Proteins c-mycras ProteinsReceptors, Urokinase Plasminogen ActivatorTumor Suppressor Protein p53Urokinase-Type Plasminogen ActivatorZBTB17 protein, human

Identifiers

PMID20123981
PMCPMC2838082
OpenAlexW2118671841

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.