Evidence map›Paper›PMID 26008968›Full record

ArticleOncotarget2015

Lemur Tyrosine Kinase 2, a novel target in prostate cancer therapy.

Kalpit Shah, Neil A Bradbury

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

17 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Lemur Tyrosine Kinases and Prostate Cancer: A Literature Review.International journal of molecular sciences · 2021
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Mechanisms of tumor cell resistance to the current targeted-therapy agents.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Review
  15. Article
  16. Article
  17. 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

2 authors at 1 institution in 1 country.

Kalpit ShahDepartment of Physiology and Biophysics, Rosalind Franklin University of Medicine & Sciences, The Chicago Medical School, North Chicago, IL 60064, USA.
Neil A BradburyDepartment of Physiology and Biophysics, Rosalind Franklin University of Medicine & Sciences, The Chicago Medical School, North Chicago, IL 60064, USA.
Rosalind Franklin University of Medicine and Science · US

Funding

Non-AR mediated DHT-promoted Bladder Cancer initiation and progressionR01CA155477 · NCI · UNIVERSITY OF ROCHESTER · PI CHANG, CHAWNSHANG · 2011 to 2015
$1.6M
Role of LMTK2 in CFTR TraffickingR01HL102208 · NHLBI · ROSALIND FRANKLIN UNIV OF MEDICINE & SCI · PI BRADBURY, NEIL A · 2011 to 2014
$1.5M
NCI NIH HHS CA155477NHLBI NIH HHS R01 HL102208
6 · The paper itself

Abstract

Progression from early forms of prostate cancer to castration-resistant disease is associated with an increase in signal transduction activity. The majority of castration-resistance cancers persist in the expression of the androgen receptor (AR), as well as androgen-dependent genes. The AR is regulated not only by it associated steroid hormone, but also by manifold regulatory and signaling molecules, including several kinases. We undertook evaluation of the role of Lemur Tyrosine Kinase 2 (LMTK2) in modulating AR activity, as several Genome Wide Association Studies (GWAS) have shown a marked association of LMTK2 activity with the development of prostate cancer. We confirm that not only is LMTK2 mRNA reduced in prostate cancer tissue, but also LMTK2 protein levels are markedly diminished. Knockdown of LMTK2 protein in prostate cell lines greatly increased the transcription of androgen-responsive genes. In addition, LMTK2 knockdown led to an increase in prostate cancer stem cell populations in LNCaP cells, indicative of increased tumorogenicity. Using multiple approaches, we also demonstrate that LMTK2 interacts with the AR, thus putting LMTK2 as a component of a signaling complex modulating AR activity. Our finding that LMTK2 is a negative regulator of AR activity defines a novel cellular pathway for activation of AR-responsive genes in castrate resistant-prostate cancer. Moreover, pharmacologic manipulation of LMTK2 activity will provide a novel therapeutic target for more effective treatments for patients with castrate-resistant prostate cancer.

Indexed as

AnimalsCell Line, TumorCell ProliferationDisease ProgressionHEK293 CellsHumansLemurMaleMolecular Targeted TherapyProstatic NeoplasmsProstatic Neoplasms, Castration-ResistantReceptors, AndrogenSignal TransductionTYK2 KinaseReceptors, AndrogenTYK2 Kinaseandrogen receptorcastrate resistant prostate cancerkinasesLMTK2prostate cancer

Identifiers

PMID26008968
PMCPMC4546463
OpenAlexW2097455736

What OpenQuestion holds

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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.