Evidence map›Paper›PMID 21408190›Full record

ArticlePloS one2011

Tyrosine kinase ETK/BMX is up-regulated in bladder cancer and predicts poor prognosis in patients with cystectomy.

Shengjie Guo, Feng Sun, Zhiyong Guo, Wei Li, Alan Alfano, Hegang Chen, Clara E Magyar, Jiaoti Huang, Toby C Chai, Shaopeng Qiu and 1 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.2field-weighted citation impact, top 9% 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

19 citing papers in PubMed, 30 citations in OpenAlex.

  1. Targeting the BMX in cancer: molecular mechanisms and emerging therapeutic strategies.Journal of enzyme inhibition and medicinal chemistry · 2026
    Review
  2. Review
  3. Article
  4. Review
  5. Review
  6. Role of tyrosine kinases in bladder cancer progression: an overview.Cell communication and signaling : CCS · 2020
    Review
  7. Nuclear localization of the tyrosine kinase BMX mediates VEGFR2 expression.Journal of cellular and molecular medicine · 2020
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. The expression and role of tyrosine kinase ETK/BMX in renal cell carcinoma.Journal of experimental & clinical cancer research : CR · 2014
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. 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

11 authors at 3 institutions in 2 countries.

Shengjie GuoDepartment of Pharmacology and Experimental Therapeutics and The Greenebaum Cancer Center, University of Maryland School of Medicine, Baltimore, Maryland, United States of America.
Feng Sun
Zhiyong Guo
Wei Li
Alan Alfano
Hegang Chen
Clara E Magyar
Jiaoti Huang
Toby C Chai
Shaopeng Qiu
Yun Qiu
University of Maryland, Baltimore · USSun Yat-sen University · CNUniversity of California, Los Angeles · US

Funding

Molecular Mechanisms of Hormone-independence of Prostate CancerR01CA106504 · NCI · UNIVERSITY OF MARYLAND BALTIMORE · PI QIU, YUN · 2005 to 2015
$2.8M
NCI NIH HHS CA106504NCI NIH HHS R01 CA106504
6 · The paper itself

Abstract

Deregulation of the non-receptor tyrosine kinase ETK/BMX has been reported in several solid tumors. In this report, we demonstrated that ETK expression is progressively increased during bladder cancer progression. We found that down-regulation of ETK in bladder cancer cells attenuated STAT3 and AKT activity whereas exogenous overexpression of ETK had opposite effects, suggesting that deregulation of ETK may attribute to the elevated activity of STAT3 and AKT frequently detected in bladder cancer. The survival, migration and invasion of bladder cancer cells were significantly compromised when ETK expression was knocked down by a specific shRNA. In addition, we showed that ETK localizes to mitochondria in bladder cancer cells through interacting with Bcl-XL and regulating ROS production and drug sensitivity. Therefore, ETK may play an important role in regulating survival, migration and invasion by modulating multiple signaling pathways in bladder cancer cells. Immunohistochemistry analysis on tissue microarrays containing 619 human bladder tissue samples shows that ETK is significantly upregulated during bladder cancer development and progression and ETK expression level predicts the survival rate of patients with cystectomy. Taken together, our results suggest that ETK may potentially serve as a new drug target for bladder cancer treatment as well as a biomarker which could be used to identify patients with higher mortality risk, who may be benefited from therapeutics targeting ETK activity.

Indexed as

CystectomyUp-Regulationbcl-X ProteinCell Line, TumorCell MovementCell SurvivalHumansMitochondriaMultivariate AnalysisNeoplasm InvasivenessPrognosisProportional Hazards ModelsProtein BindingProtein TransportProtein-Tyrosine KinasesSurvival Analysisbcl-X ProteinBMX protein, humanProtein-Tyrosine Kinases

Identifiers

PMID21408190
PMCPMC3049795
OpenAlexW2016143947

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.