Evidence map›Paper›PMID 19503093›Full record

ArticleOncogene2009

Frequent loss of cystatin E/M expression implicated in the progression of prostate cancer.

S M Pulukuri, B Gorantla, J A Knost, J S Rao

Open access · greenAbstract read
In one paragraph

Article in Oncogene, 2009. 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
1.0field-weighted citation impact, top 21% 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, 43 citations in OpenAlex.

  1. Review
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  10. The Role of Cysteine Cathepsins in Cancer Progression and Drug Resistance.International journal of molecular sciences · 2019
    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

4 authors at 2 institutions in 1 country.

S M PulukuriDepartment of Cancer Biology and Pharmacology, University of Illinois College of Medicine at Peoria, 61605, USA.
B Gorantla
J A Knost
J S Rao
Illinois College · USIllinois CancerCare · US

Funding

Cath B and uPAR si RNA constructs regressed glioma growthR01CA116708 · NCI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI O'BRYAN, JOHN P · 2005 to 2014
$2.9M
Inhibition of glioma tumor growth by antisense MMP-9R01NS047699 · NINDS · UNIVERSITY OF ILLINOIS AT CHICAGO · PI RAO, JASTI S. · 2003 to 2011
$2.5M
Role of uPA and uPAR in Human Glioma InvasivenessR01CA075557 · NCI · UNIVERSITY OF TEXAS MD ANDERSON CAN CTR · PI RAO, JASTI S. · 1998 to 2009
$2.3M
Growth inhibition of brain tumors by cord blood stem cellsR01NS057529 · NINDS · UNIVERSITY OF ILLINOIS AT CHICAGO · PI RAO, JASTI S. · 2006 to 2010
$1.8M
Regression of meningioma tumor growth by combination therapyR01NS061835 · NINDS · UNIVERSITY OF ILLINOIS AT CHICAGO · PI RAO, JASTI S. · 2008 to 2012
$1.7M
Inhibition of matrix proteases to sensitize medulloblastoma cells to radiationR01CA138409 · NCI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI GARTEL, ANDREI L · 2009 to 2013
$1.6M
Role of TFPI-2 in human gliomas invasivenessR01CA095058 · NCI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI RAO, JASTI S. · 2003 to 2007
$1.5M
Suppression of glioma invasion by a bicistronic constuctR01CA092393 · NCI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI RAO, JASTI S. · 2003 to 2007
$1.4M
NCI NIH HHS CA116708NCI NIH HHS CA138409NCI NIH HHS CA75557NCI NIH HHS CA92393NCI NIH HHS CA95058NCI NIH HHS R01 CA075557NCI NIH HHS R01 CA092393NCI NIH HHS R01 CA095058NCI NIH HHS R01 CA116708NCI NIH HHS R01 CA138409NINDS NIH HHS NS47699NINDS NIH HHS NS57529NINDS NIH HHS NS61835NINDS NIH HHS R01 NS047699NINDS NIH HHS R01 NS057529NINDS NIH HHS R01 NS061835
6 · The paper itself

Abstract

Cystatin E/M (CST6) is a natural inhibitor of lysosomal cysteine proteases. Recent studies have shown that experimental manipulation of CST6 expression alters the metastatic behavior of human breast cancer cells. However, the association of CST6 with prostate cancer invasion and progression remains unclear. Here, we show that CST6 is robustly expressed in normal human prostate epithelium, whereas its expression is downregulated in metastatic prostate cell lines and prostate tumor tissues. Treatment of metastatic prostate cell lines with the histone deacetylase inhibitor trichostatin A resulted in significant induction of CST6 mRNA levels and increased CST6 protein expression, indicating that epigenetic silencing may play a role in the loss of CST6 expression observed in prostate cancer. CST6 overexpression in human prostate cancer cells significantly reduced in vitro cell proliferation and matrigel invasion. Furthermore, the results from a bioluminescence tumor/metastasis model showed that the overexpression of CST6 significantly inhibits tumor growth and the incidence of lung metastasis. These results suggest that the downregulation of the CST6 gene is associated with promoter histone modifications and that this association plays an important role in prostate cancer progression during the invasive and metastatic stages of the disease.

Indexed as

Gene Expression ProfilingAcetylationAnimalsAzacitidineBlotting, WesternCell Line, TumorCell ProliferationChromatinCystatin MDecitabineDisease ProgressionDNA MethylationGene Expression Regulation, NeoplasticHistone Deacetylase InhibitorsHistonesHumansAzacitidineChromatinCST6 protein, humanCystatin MDecitabineHistone Deacetylase InhibitorsHistonesHydroxamic Acidstrichostatin A

Identifiers

PMID19503093
PMCPMC2722685
OpenAlexW2001157528

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.