Evidence map›Paper›PMID 13679857›Full record

ArticleOncogene2003

Mitogenic effects of gastrin-releasing peptide in head and neck squamous cancer cells are mediated by activation of the epidermal growth factor receptor.

Vivian Wai Yan Lui, Sufi Mary Thomas, Qing Zhang, Abbey Lynn Wentzel, Jill Marie Siegfried, Joyce Yan Li, Jennifer Rubin Grandis

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
1.9field-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

45 citing papers in PubMed, 82 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. NSAIDs OvercomeCancers · 2022
    Article
  5. Review
  6. Article
  7. P2YOral oncology · 2020
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. G Protein-Coupled Receptor Signaling in Stem Cells and Cancer.International journal of molecular sciences · 2016
    Review
  13. iRhoms; Its Functions and Essential Roles.Biomolecules & therapeutics · 2016
    Article
  14. Review
  15. Article
  16. 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

7 authors at 2 institutions in 1 country.

Vivian Wai Yan LuiDepartment of Otolaryngology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA.
Sufi Mary Thomas
Qing Zhang
Abbey Lynn Wentzel
Jill Marie Siegfried
Joyce Yan Li
Jennifer Rubin Grandis
University of Pittsburgh · USUPMC Hillman Cancer Center · US

Funding

Vitamin D3 Modulation of Inflammation and Lung Cancer RiskP50CA090440 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI DACIC, SANJA · 2001 to 2015
$34.6M
Serum Proteomic Biomarkers for Colon &Pancreatic CancerU01CA084968 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI BIGBEE, WILLIAM L · 1999 to 2009
$6.4M
Targeting the HGF/c-Met Pathway in Lung CancerR01CA079882 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI SIEGFRIED, JILL M · 1999 to 2013
$3.7M
NCI NIH HHS P50CA90440NCI NIH HHS R01CA79882NCI NIH HHS U01CA84968
6 · The paper itself

Abstract

Head and neck squamous cell carcinomas (HNSCC) are characterized by upregulation of the epidermal growth factor receptor (EGFR), where EGFR serves as a potential therapeutic target. We previously reported that a gastrin-releasing peptide/gastrin-releasing peptide receptor (GRP/GRPR) autocrine growth pathway is activated early in HNSCC carcinogenesis. In the present study, we examined the mechanism of EGFR activation by GRP/GRPR in HNSCC proliferation. In HNSCC cells that express elevated levels of both GRPR and EGFR, we found that GRP induced rapid phosphorylation of EGFR as well as p44/42-MAPK activation. Using several EGFR-specific tyrosine kinase inhibitors and cells derived from EGFR knockout mice, we demonstrated that GRP-induced p44/42-MAPK activation was dependent upon EGFR activation. Further investigation demonstrated that cleavage of transforming growth factor-alpha (TGF-alpha) by matrix metalloproteinases mediated GRP-induced MAPK activation. In addition, HNSCC proliferation stimulated by GRP was eliminated upon specific inhibition of EGFR or MEK, and GRP failed to stimulate proliferation in EGFR-deficient cells. These results imply that the mitogenic effects of GRP in HNSCC are mediated by extracellular release of TGF-alpha and require the activation of an EGFR-dependent MEK/MAPK-dependent pathway.

Indexed as

MAP Kinase Kinase Kinase 1AnimalsCarcinoma, Squamous CellCell DivisionEnzyme ActivationEnzyme InhibitorsErbB ReceptorsFibroblastsGastrin-Releasing PeptideHead and Neck NeoplasmsHumansMiceMice, KnockoutMitogen-Activated Protein Kinase 3Mitogen-Activated Protein KinasesMitogensEnzyme InhibitorsErbB ReceptorsGastrin-Releasing PeptideMAP3K1 protein, humanMap3k1 protein, mouseMAP Kinase Kinase Kinase 1Mitogen-Activated Protein Kinase 3Mitogen-Activated Protein KinasesMitogensProtein Serine-Threonine KinasesReceptors, Bombesin

Identifiers

PMID13679857
OpenAlexW2000308166

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.