Evidence map›Paper›PMID 15735691›Full record

ArticleOncogene2005

Y-box-binding protein 1 confers EGF independence to human mammary epithelial cells.

Isabelle M Berquin, Bing Pang, Michele L Dziubinski, Latanya M Scott, Yong Q Chen, Garry P Nolan, Stephen P Ethier

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

32 citing papers in PubMed, 66 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Y-box binding protein 1 augments sorafenib resistanceWorld journal of gastroenterology · 2021
    Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Transcription factors that interact with p53 and Mdm2.International journal of cancer · 2016
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Expression of Y-Box-binding protein 1 in Chinese patients with breast cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2012
    Article
  18. YB-1, the E2F pathway, and regulation of tumor cell growth.Journal of the National Cancer Institute · 2012
    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 3 institutions in 1 country.

Isabelle M BerquinDepartment of Pathology, Wake Forest University, Winston-Salem, NC 27157, USA. iberquin@wfubmc.edu
Bing Pang
Michele L Dziubinski
Latanya M Scott
Yong Q Chen
Garry P Nolan
Stephen P Ethier
Wake Forest University · USUniversity of Michigan–Ann Arbor · USStanford University · US

Funding

EXPRESSION CLONING OF NOVEL BREAST CANCER ONCOGENESR01CA077416 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ETHIER, STEPHEN P. · 1999 to 2002
$665k
NCI NIH HHS R01 CA77416
6 · The paper itself

Abstract

The epidermal growth factor receptor (EGFR) is linked to poor outcome in breast cancer, and resistance to hormonal therapy is often accompanied by activation of growth factor receptors. To investigate the mechanism(s) by which EGFR becomes activated in breast cancer, we screened a cDNA expression library for genes that mediate EGF-independent proliferation of human mammary epithelial cells (HMECs). We isolated the NSEP1 cDNA encoding Y-box-binding protein 1 (YB-1), a multifunctional transcriptional and translational regulator. This cDNA conferred growth factor independence to HMECs. YB-1-transduced cells overexpressed EGFR, but ErbB-2 (Her-2/neu) levels were unchanged. Moreover, EGFR was constitutively phosphorylated in the absence of exogenous ligand. In these cells, an EGFR-blocking antibody failed to inhibit proliferation, conditioned medium activity could not be detected, and the synthesis of EGFR ligands was reduced compared to parental cells. This suggests that EGFR is activated in a ligand-independent fashion. However, cell growth could be blocked with an ErbB kinase inhibitor, indicating that EGFR signaling plays a major role in YB-1-induced growth factor independence. Taken together, our results demonstrate that YB-1 overexpression can induce EGF independence in HMECs via activation of the EGFR pathway. This could represent one of the mechanisms by which YB-1 contributes to breast tumor aggressiveness.

Indexed as

AllelesBlotting, NorthernBreastBreast NeoplasmsCCAAT-Enhancer-Binding ProteinsCell Line, TumorCell ProliferationCells, CulturedCloning, MolecularDNA, ComplementaryEpidermal Growth FactorEpithelial CellsErb-b2 Receptor Tyrosine KinasesErbB ReceptorsGene LibraryHumansCCAAT-Enhancer-Binding ProteinsDNA, ComplementaryEpidermal Growth FactorErb-b2 Receptor Tyrosine KinasesErbB ReceptorsLigandsNFI Transcription FactorsTranscription FactorsY-Box-Binding Protein 1

Identifiers

PMID15735691
OpenAlexW2066289540

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.