Evidence map›Paper›PMID 17786183›Full record

ArticleNeoplasia (New York, N.Y.)2007

Expression and function of the human androgen-responsive gene ADI1 in prostate cancer.

Shane W Oram, Junkui Ai, Gina M Pagani, Moira R Hitchens, Jeffrey A Stern, Scott Eggener, Michael Pins, Wuhan Xiao, Xiaoyan Cai, Riffat Haleem and 4 more

Open access · goldAbstract readComparative Study
In one paragraph

Article in Neoplasia (New York, N.Y.), 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

29 citing papers in PubMed, 39 citations in OpenAlex.

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  15. Dual chemistry catalyzed by human acireductone dioxygenase.Protein engineering, design & selection : PEDS · 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

14 authors at 4 institutions in 1 country.

Shane W OramDepartment of Urology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.
Junkui Ai
Gina M Pagani
Moira R Hitchens
Jeffrey A Stern
Scott Eggener
Michael Pins
Wuhan Xiao
Xiaoyan Cai
Riffat Haleem
Feng Jiang
Thomas C Pochapsky
Lizbeth Hedstrom
Zhou Wang
Northwestern University · USBrandeis University · USUPMC Hillman Cancer Center · USUniversity of Pittsburgh Medical Center · US

Funding

SUPPRESSIVE ROLE OF ANDROGEN RESPONSE GENE CALRETICULIN IN PROSTATE CANCERP50CA090386 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI LEE, CHUNG · 2001 to 2013
$25.1M
Role of U19/Eaf2 in androgen-dependent prostate homeostasisR01DK051193 · NIDDK · NORTHWESTERN UNIVERSITY AT CHICAGO · PI WANG, ZHOU · 1997 to 2006
$1.7M
A Novel CO-producing MetalloenzymeR01GM067786 · NIGMS · BRANDEIS UNIVERSITY · PI POCHAPSKY, THOMAS CHARLES · 2003 to 2006
$882k
NCI NIH HHS P50 CA090386NCI NIH HHS P50 CA90386NIDDK NIH HHS R01 DK051193NIDDK NIH HHS R01 DK51193NIGMS NIH HHS R01 GM067786
6 · The paper itself

Abstract

We have previously identified an androgen-responsive gene in rat prostate that shares homology with the aci-reductone dioxygenase (ARD/ARD') family of metal-binding enzymes involved in methionine salvage. We found that the gene, aci-reductone dioxygenase 1 (ADI1), was downregulated in prostate cancer cells, whereas enforced expression of rat Adi1 in these cells caused apoptosis. Here we report the characterization of human ADI1 in prostate cancer. Androgens induced ADI1 expression in human prostate cancer LNCaP cells, which was not blocked by cycloheximide, indicating that ADI1 is a primary androgen-responsive gene. In human benign prostatic hyperplasia specimens, epithelial cells expressed ADI1. Immunohistochemistry of prostate tumor tissue microarrays showed that benign regions expressed more ADI1 than tumors, suggesting a suppressive role for ADI1 in prostate cancer. Bacterial lysates containing recombinant ADI1 produced a five-fold increase in aci-reductone decay over controls, demonstrating that ADI1 has ARD activity. We generated point mutations at key residues in the metal-binding site of ADI1 to disrupt ARD function, and we found that these mutations did not affect intracellular localization, apoptosis, or colony formation suppression in human prostate cancer cells. Collectively, these observations argue that ADI1 may check prostate cancer progression through apoptosis and that this activity does not require metal binding.

Indexed as

AndrogensApoptosisCarrier ProteinsCell Line, TumorDioxygenasesGene Expression Regulation, NeoplasticHumansMaleMetalsProstatic NeoplasmsProtein BindingADI1 protein, humanAndrogensCarrier ProteinsDioxygenasesMetalsaci-reductone dioxygenaseADI1androgen-responsive geneapoptosisprostate cancer

Identifiers

PMID17786183
PMCPMC1950434
OpenAlexW2038916593

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.