Evidence map›Paper›PMID 19444856›Full record

ArticleThe Prostate2009

Expression level and DNA methylation status of glutathione-S-transferase genes in normal murine prostate and TRAMP tumors.

Cory K Mavis, Shannon R Morey Kinney, Barbara A Foster, Adam R Karpf

Open access · greenAbstract read
In one paragraph

Article in The Prostate, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

14 citing papers in PubMed, 31 citations in OpenAlex.

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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

4 authors at 1 institution in 1 country.

Cory K MavisDepartment of Pharmacology and Therapeutics, Roswell Park Cancer Institute, Buffalo, New York 14263, USA.
Shannon R Morey Kinney
Barbara A Foster
Adam R Karpf
Roswell Park Comprehensive Cancer Center · US

Funding

Two-Spirit Films in Indigenous Cancer HealthP30CA016056 · NCI · ROSWELL PARK CANCER INSTITUTE CORP · PI MARK G FRATTINI · 1985 to 2026
$116.6M
DRUG DEVELOPMENT AND CANCER TREATMENTST32CA009072 · NCI · ROSWELL PARK CANCER INSTITUTE CORP · PI JOHNSON, CANDACE S · 1985 to 2014
$2.3M
Green tea-mediated inhibition of aberrant DNA hypermethylation in prostate cancerR21CA128062 · NCI · ROSWELL PARK CANCER INSTITUTE CORP · PI KARPF, ADAM R · 2006 to 2007
$294k
NCI NIH HHS 5T32CA009072NCI NIH HHS CA16056NCI NIH HHS P30 CA016056NCI NIH HHS R21 CA128062NCI NIH HHS R21CA128062NCI NIH HHS T32 CA009072
6 · The paper itself

Abstract

backgroundGlutathione-S-transferase (Gst) genes are downregulated in human prostate cancer, and GSTP1 silencing is mediated by promoter DNA hypermethylation in this malignancy. We examined Gst gene expression and Gst promoter DNA methylation in normal murine prostates and Transgenic Adenocarcinoma of Mouse Prostate (TRAMP) tumors.

methodsPrimary and metastatic tumors were obtained from TRAMP mice, and normal prostates were obtained from strain-matched WT mice (n = 15/group). Quantitative real-time RT-PCR was used to measure GstA4, GstK1, GstM1, GstO1, and GstP1 mRNA expression, and Western blotting and immunohistochemical staining was used to measure GstM1 and GstP1 protein expression. MassARRAY Quantitative Methylation Analysis was used to measure DNA methylation of the 5' CpG islands of GstA4, GstK1, GstM1, GstO1, and GstP1. TRAMP-C2 cells were treated with the epigenetic remodeling drugs decitabine and trichostatin A (TSA) alone and in combination, and Gst gene expression was measured.

resultsOf the genes analyzed, GstM1 and GstP1 were expressed at highest levels in normal prostate. All five Gst genes showed greatly reduced expression in primary tumors compared to normal prostate, but not in tumor metastases. Gst promoter methylation was unchanged in TRAMP tumors compared to normal prostate. Combined decitabine + TSA treatment significantly enhanced the expression of 4/5 Gst genes in TRAMP-C2 cells.

conclusionsGst genes are extensively downregulated in primary but not metastatic TRAMP tumors. Promoter DNA hypermethylation does not appear to drive Gst gene repression in TRAMP primary tumors; however, pharmacological studies using TRAMP cells suggest the involvement of epigenetic mechanisms in Gst gene repression.

Indexed as

DNA MethylationAdenocarcinomaAnimalsAntimetabolites, AntineoplasticAzacitidineCell Line, TumorCpG IslandsDecitabineDrug CombinationsGene Expression Regulation, EnzymologicGene Expression Regulation, NeoplasticGene SilencingGlutathione S-Transferase piGlutathione TransferaseHydroxamic AcidsMaleAntimetabolites, AntineoplasticAzacitidineDecitabineDrug CombinationsGlutathione S-Transferase piGlutathione TransferaseGstp1 protein, mouseHydroxamic AcidsRNA, Messengertrichostatin A

Identifiers

PMID19444856
PMCPMC2836025
OpenAlexW1966766360

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Registered trials

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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.