Evidence map›Paper›PMID 12606946›Full record

ArticleOncogene2003

Osteopontin-induced migration of human mammary epithelial cells involves activation of EGF receptor and multiple signal transduction pathways.

Alan B Tuck, Charulata Hota, Sylvia M Wilson, Ann F Chambers

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 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
8.1field-weighted citation impact, top 2% 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

49 citing papers in PubMed, 127 citations in OpenAlex.

  1. Review
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  14. Role of osteopontin in the pathophysiology of cancer.Matrix biology : journal of the International Society for Matrix Biology · 2014
    Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. Matrikine and matricellular regulators of EGF receptor signaling on cancer cell migration and invasion.Laboratory investigation; a journal of technical methods and pathology · 2014
    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

4 authors at 2 institutions in 1 country.

Alan B TuckDepartment of Pathology, London Health Sciences Centre, University of Western Ontario, London, Ontario, Canada. atuck@uwo.ca
Charulata Hota
Sylvia M Wilson
Ann F Chambers
Western University · CAOttawa Regional Cancer Foundation · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Osteopontin (OPN) is a secreted, integrin-binding glycophosphoprotein that has been implicated in breast cancer. We previously showed that OPN-induced cell migration of mammary epithelial cells (MEC) depends on binding to cell surface integrins and involves activation of the hepatocyte growth factor (HGF) receptor, Met. Here, we show that OPN-induced migration of MEC also requires activation of the epidermal growth factor (EGF) pathway. Synergism was seen between EGF and OPN in inducing cell migration. Furthermore, incubation of cells with exogenous OPN increased ligand (TGFalpha> EGF) and EGF receptor (EGFR) mRNA expression, as well as EGFR kinase activity. Treatment of cells with anti-TGFalpha or anti-EGFR antibody, or with tyrphostin-25 (EGFR inhibitor), significantly impaired the cell migration response to OPN. Other more broad-spectrum tyrosine kinase inhibitors and the growth factor/ receptor interaction inhibitor, suramin, also inhibited OPN-induced migration. Using specific signal transduction pathway inhibitors, we have screened for involvement of MEK (MAP kinase kinase), phosphatidylinositol 3-kinase, phospholipase C (PLC), and protein kinase C (PKC). Results implicated all of these pathways in OPN-induced cell migration, the most pronounced effect being seen with PLC and PKC inhibitors. These results suggest that induction of MEC migration by OPN involves a cascade of events including at least two growth factor/receptor pathways and multiple downstream signal transduction pathways. A number of potential targets are thus provided for strategies aimed at blocking the malignancy-promoting effects of OPN.

Indexed as

AdenocarcinomaBreastBreast NeoplasmsCell MovementEnzyme InhibitorsEpidermal Growth FactorEpithelial CellsErbB ReceptorsFemaleGene Expression Regulation, NeoplasticHumansMAP Kinase Signaling SystemNeoplasm ProteinsOligonucleotides, AntisenseOsteopontinPhosphatidylinositol 3-KinasesEnzyme InhibitorsEpidermal Growth FactorErbB ReceptorsNeoplasm ProteinsOligonucleotides, AntisenseOsteopontinPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProtein Kinase CProto-Oncogene Proteins c-metRecombinant Fusion ProteinsRecombinant ProteinsRNA, MessengerSialoglycoproteinsSPP1 protein, humanTransforming Growth Factor alphaType C Phospholipases

Identifiers

PMID12606946
OpenAlexW2063152874

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.