Evidence map›Paper›PMID 23538858›Full record

ArticleMolecular cancer research : MCR2013

ERK and AKT signaling drive MED1 overexpression in prostate cancer in association with elevated proliferation and tumorigenicity.

Feng Jin, Shazia Irshad, Wei Yu, Madesh Belakavadi, Marina Chekmareva, Michael M Ittmann, Cory Abate-Shen, Joseph D Fondell

Open access · greenAbstract read
In one paragraph

Article in Molecular cancer research : MCR, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

24 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. 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

8 authors at 3 institutions in 1 country.

Feng JinDepartment of Physiology and Biophysics, Robert Wood Johnson Medical School, UMDNJ, 683 Hoes Lane, Piscataway, New Jersey 08854, USA.
Shazia Irshad
Wei Yu
Madesh Belakavadi
Marina Chekmareva
Michael M Ittmann
Cory Abate-Shen
Joseph D Fondell
Baylor College of Medicine · USColumbia University · USJohnson University · US

Funding

Elucidation of cancer pathways and druggable targets using mouse models.U01CA084294 · NCI · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI ABATE-SHEN, CORY · 1999 to 2013
$11.4M
Roles for Nkx3.1 in Prostate Cancer InitiationP01CA154293 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI CORDON-CARDO, CARLOS · 2011 to 2015
$6.5M
NCI NIH HHS P01 CA154293NCI NIH HHS U01 CA084294
6 · The paper itself

Abstract

MED1 is a key coactivator of the androgen receptor (AR) and other signal-activated transcription factors. Whereas MED1 is overexpressed in prostate cancer cell lines and is thought to coactivate distinct target genes involved in cell-cycle progression and castration-resistant growth, the underlying mechanisms by which MED1 becomes overexpressed and its oncogenic role in clinical prostate cancer have remained unclear. Here, we report that MED1 is overexpressed in the epithelium of clinically localized human prostate cancer patients, which correlated with elevated cellular proliferation. In a Nkx3.1:Pten mutant mouse model of prostate cancer that recapitulates the human disease, MED1 protein levels were markedly elevated in the epithelium of both invasive and castration-resistant adenocarcinoma prostate tissues. Mechanistic evidence showed that hyperactivated ERK and/or AKT signaling pathways promoted MED1 overexpression in prostate cancer cells. Notably, ectopic MED1 overexpression in prostate cancer xenografts significantly promoted tumor growth in nude mice. Furthermore, MED1 expression in prostate cancer cells promoted the expression of a number of novel genes involved in inflammation, cell proliferation, and survival. Together, these findings suggest that elevated MED1 is a critical molecular event associated with prostate oncogenesis.

Indexed as

Signal TransductionAnimalsCarcinogenesisCell CycleCell Line, TumorCell ProliferationCell SurvivalDisease Models, AnimalExtracellular Signal-Regulated MAP KinasesGene Expression Regulation, NeoplasticHomeodomain ProteinsHumansInflammationMaleMediator Complex Subunit 1MiceExtracellular Signal-Regulated MAP KinasesHomeodomain ProteinsMED1 protein, humanMed1 protein, mouseMediator Complex Subunit 1Nkx3-1 protein, mouseProto-Oncogene Proteins c-mycPTEN PhosphohydrolasePten protein, mouseTranscription Factors

Identifiers

PMID23538858
PMCPMC5838364
OpenAlexW2137199913

What OpenQuestion holds

Textmetadata
LicenceTDM
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.