Evidence map›Paper›PMID 18223692›Full record

ArticleOncogene2008

Src kinase potentiates androgen receptor transactivation function and invasion of androgen-independent prostate cancer C4-2 cells.

M Asim, I A Siddiqui, B B Hafeez, A Baniahmad, H Mukhtar

Open access · bronzeAbstract read
In one paragraph

Article in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
6.1field-weighted citation impact, top 4% 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

56 citing papers in PubMed, 110 citations in OpenAlex.

  1. Article
  2. Review
  3. Androgen receptor and estrogen receptor variants in prostate and breast cancers.The Journal of steroid biochemistry and molecular biology · 2024
    Review
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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 2 institutions in 2 countries.

M AsimDepartment of Dermatology, University of Wisconsin, Madison, WI 53706, USA.
I A Siddiqui
B B Hafeez
A Baniahmad
H Mukhtar
University of Wisconsin–Madison · USUniversity of Eastern Finland · FI

Funding

The Role of JunD in Androgen-Induced Changes in Prostate Gland Redox StateP50DK065303 · NIDDK · UNIVERSITY OF WISCONSIN-MADISON · PI BUSHMAN, WADE A. · 2003 to 2007
$4.0M
Green Tea in Chemoprevention of Prostate CancerR01CA078809 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI MUKHTAR, HASAN · 1999 to 2008
$1.9M
Molecular Targets for Prevention of Prostate Cancer by Green TeaR01CA101039 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI MUKHTAR, HASAN · 2003 to 2007
$1.6M
Pomegranate for Chemoprevention and Chemotherapy of Prostate CancerR01CA120451 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI MUKHTAR, HASAN · 2007 to 2011
$1.4M
NCI NIH HHS R01 CA078809NCI NIH HHS R01 CA101039NCI NIH HHS R01CA101039NCI NIH HHS R01 CA120451NCI NIH HHS R01CA120451NCI NIH HHS R01CA78809NIDDK NIH HHS P50 DK065303NIDDK NIH HHS P50DK065303-01
6 · The paper itself

Abstract

Prostate cancer is one of the most prominent malignancies of elderly men in many Western countries including Europe and the United States with increasing trend worldwide. The growth of normal prostate as well as of prostate carcinoma cells depends on functional androgen receptor (AR) signaling. AR manifests the biological actions of androgens and its transcriptional activity is known to be influenced by signal transduction pathways. Here we show that Src, a nonreceptor tyrosine kinase, is overexpressed in androgen-independent prostate carcinoma C4-2 cells. Interestingly, the expression of Src was found to progressively increase (up to threefold) in transgenic adenocarcinoma of mouse prostate mice as a function of age and cancer progression. Blocking Src kinase function by a specific inhibitor, PP2, resulted in decreased AR transactivation function on two different reporters, mouse mammary tumor virus (MMTV) and prostate-specific antigen (PSA). Consistent with this, overexpression of a functional Src mutant also led to a dramatic decrease in AR transactivation potential in a hormone-dependent manner. Interference with Src function in C4-2 cells led to decreased recruitment of AR on the target gene PSA enhancer and also resulted in the abrogation of hormone-dependent PSA transcript induction. Src inhibition also led to a dramatic decrease in the cell invasion in addition to decreasing the cellular growth. We suggest that targeting Src kinase could be an effective strategy to inhibit prostate cancer growth and metastasis.

Indexed as

Gene Expression Regulation, EnzymologicGene Expression Regulation, NeoplasticAndrogensAnimalsCell Line, TumorHumansMaleMiceMice, TransgenicModels, BiologicalNeoplasm InvasivenessProstatic NeoplasmsReceptors, AndrogenTranscription, GeneticTransgenesAndrogensReceptors, Androgen

Identifiers

PMID18223692
PMCPMC8445586
OpenAlexW2005528673

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.