Evidence map›Paper›PMID 14676838›Full record

ArticleOncogene2004

The role of tyrosine kinase Etk/Bmx in EGF-induced apoptosis of MDA-MB-468 breast cancer cells.

Kai-Yun Chen, Li-Ming Huang, Hsing-Jien Kung, David K Ann, Hsiu-Ming Shih

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
0.6field-weighted citation impact, top 38% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.

  1. Pooled it
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  5. Article
  6. EGFR-mediated apoptosis via STAT3.Experimental cell research · 2017
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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

5 authors at 4 institutions in 2 countries.

Kai-Yun ChenGraduate Institute of Life Sciences, National Defense Medical Center, Taipei, Taiwan, ROC.
Li-Ming Huang
Hsing-Jien Kung
David K Ann
Hsiu-Ming Shih
National Health Research Institutes · TWNational Defense Medical Center · TWSouthern California University for Professional Studies · USUniversity of California, Davis · US

Funding

MOLECULAR PROGRAMMING OF SALIVARY GLAND GENE EXPRESSIONR01DE010742 · NIDCR · UNIVERSITY OF SOUTHERN CALIFORNIA · PI ANN, DAVID K. · 1993 to 2013
$5.1M
Molecular Hierarchies in Salivary Adaptive ResponsesR01DE014183 · NIDCR · UNIVERSITY OF SOUTHERN CALIFORNIA · PI ANN, DAVID K. · 2001 to 2011
$3.3M
ERBB KINASE ACTIVATION AND TRANSFORMATIONR01CA039207 · NCI · UNIVERSITY OF CALIFORNIA DAVIS · PI KUNG, HSING-JIEN · 1986 to 2004
$1.5M
ERBB KINASE ACTIVATION AND TRANSFORMATIONR37CA039207 · NCI · UNIVERSITY OF CALIFORNIA DAVIS · PI KUNG, HSING-JIEN · 1991 to 1999
–
NCI NIH HHS CA39207NIDCR NIH HHS DE14183NIDCR NIH HHS R01 DE10742PHS HHS 91574
6 · The paper itself

Abstract

Etk/Bmx, a member of the Tec family of tyrosine kinases, mediates various signaling pathways and confers several cellular functions. In the present study, we have explored the functional role of Etk in mediating EGF-induced apoptosis, using MDA-MB-468 cell line as a model. We first demonstrated that EGF treatment induces Etk tyrosine phosphorylation in both HeLa and MDA-MB-468 cells. Overexpression of Etk by recombinant adenovirus in MDA-MB-468 cells potentiates the extent of EGF-induced cell apoptosis. The observed Etk-enhanced MDA-MB-468 cell apoptosis is associated with the Stat1 activation, as demonstrated by electrophoresis mobility shift assays and reporter gene assays. By contrast, a kinase domain deletion mutant EtkDeltaK, functioning as a dominant-negative mutant, ameliorates EGF-induced Stat1 activation and apoptosis in MDA-MB-468 cells. To explore whether the activated Etk alone is sufficient for inducing apoptosis, a conditionally activated Etk (DeltaEtk-ER), a chimeric fusion protein of PH domain-truncated Etk and ligand-binding domain of estrogen receptor, was introduced into MDA-MB-468 cells. Upon beta-estradiol ligand activation, the DeltaEtk-ER could stimulate Stat1 activity and confer cell apoptosis independent of EGF treatment. Taken together, our findings indicate that Etk is a downstream signaling molecule of EGF receptor and suggest that Etk activation is essential for transducing the EGF-induced apoptotic signaling.

Indexed as

ApoptosisBase SequenceBreast NeoplasmsCell Line, TumorDNA PrimersEnzyme ActivationEpidermal Growth FactorFemaleHumansMembrane ProteinsMutagenesisProtein-Tyrosine KinasesRecombinant ProteinsBMX protein, humanDNA PrimersEpidermal Growth FactorMembrane ProteinsProtein-Tyrosine KinasesRecombinant Proteins

Identifiers

PMID14676838
OpenAlexW1982104751

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.