Evidence map›Paper›PMID 21489997›Full record

ArticleThe Journal of biological chemistry2011

Met receptors induce Sam68-dependent cell migration by activation of alternate extracellular signal-regulated kinase family members.

Alessia Locatelli, Carol A Lange

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

22 citing papers in PubMed, 48 citations in OpenAlex.

  1. Role of Sam68 in different types of cancer (Review).International journal of molecular medicine · 2025
    Review
  2. Review
  3. Role of Sam68 as an adaptor protein in inflammatory signaling.Cellular and molecular life sciences : CMLS · 2024
    Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Leptin, Adiponectin, and Sam68 in Bone Metastasis from Breast Cancer.International journal of molecular sciences · 2020
    Review
  12. Impact of ERK5 on the Hallmarks of Cancer.International journal of molecular sciences · 2019
    Review
  13. Article
  14. Article
  15. Role of Sam68 in post-transcriptional gene regulation.International journal of molecular sciences · 2013
    Review
  16. Article
  17. Review
  18. Review
  19. Review
  20. Review
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

2 authors at 1 institution in 1 country.

Alessia LocatelliDepartment of Medicine (Division of Hematology, Oncology, and Transplantation), Masonic Cancer Center, University of Minnesota, Minneapolis, Minnesota 55455, USA.
Carol A Lange
Palmetto Hematology Oncology · US

Funding

Brk signal transduction in breast cancerR01CA107547 · NCI · UNIVERSITY OF MINNESOTA · PI LANGE, CAROL A · 2007 to 2011
$1.3M
NCI NIH HHS CA107547NCI NIH HHS R01 CA107547
6 · The paper itself

Abstract

The hepatocyte growth factor (HGF)/Met receptor signaling pathway is deregulated in diverse human malignancies and plays a central role in oncogenesis, tumor progression, and invasive cancer growth. Similarly, altered expression and splicing (i.e. inclusion of variant exon 5, "v5") of the cell adhesion marker, CD44, is associated with advanced cancer phenotypes. We sought to further understand how HGF regulates CD44v5 expression. Immortalized nontumorigenic keratinocyte (HaCaT) cells abundantly express both Met receptors and CD44v5 transmembrane glycoproteins. HGF stimulated CD44v5 protein expression and HaCaT cell migration; these events required activation of the ERK1/2 MAPK module and Sam68, a protein involved in RNA processing, splicing, and v5 inclusion. Similar to HaCaT cells, highly migratory MDA-MB-231 breast cancer cells also required Sam68 expression for HGF-induced migration. However, MDA-MB-231 cell migration occurred independently of ERK1/2 and CD44v5 expression and instead required ERK5 signaling to Sam68. Phospho-mutant, but not WT-Sam68, blocked HGF-induced cell migration in both cell types; MDA-MB-435 cells behaved similarly. These results suggest that Sam68 acts as a convergence point for ERK signaling to cell migration; blockade of phospho-Sam68 may provide a new avenue for therapeutic inhibition of metastatic cancers.

Indexed as

Adaptor Proteins, Signal TransducingCell AdhesionCell Line, TumorCell MembraneCell MovementDNA-Binding ProteinsExtracellular Signal-Regulated MAP KinasesGlycoproteinsHepatocyte Growth FactorHumansHyaluronan ReceptorsKeratinocytesModels, BiologicalNeoplasm MetastasisProto-Oncogene Proteins c-metRNA-Binding ProteinsAdaptor Proteins, Signal TransducingCD44v5 antigenDNA-Binding ProteinsExtracellular Signal-Regulated MAP KinasesGlycoproteinsHepatocyte Growth FactorHyaluronan ReceptorsKHDRBS1 protein, humanProto-Oncogene Proteins c-metRNA-Binding Proteins

Identifiers

PMID21489997
PMCPMC3122167
OpenAlexW1968027570

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.