Evidence map›Paper›PMID 20132547›Full record

ArticleMolecular cancer2010

Prosaposin down-modulation decreases metastatic prostate cancer cell adhesion, migration, and invasion.

Siyi Hu, Nathalie Delorme, Zhenzhen Liu, Tao Liu, Cruz Velasco-Gonzalez, Jone Garai, Ashok Pullikuth, Shahriar Koochekpour

Open access · goldAbstract read
In one paragraph

Article in Molecular cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 13% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 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

8 authors at 1 institution in 1 country.

Siyi HuStanley S Scott Cancer Center, School of Medicine, Louisiana State University Health Sciences Center, New Orleans, LA 70112, USA.
Nathalie Delorme
Zhenzhen Liu
Tao Liu
Cruz Velasco-Gonzalez
Jone Garai
Ashok Pullikuth
Shahriar Koochekpour
Louisiana State University Health Sciences Center New Orleans · US

Funding

TUMOR MICROENVIRONMENT AND B CELL LYMPHOMASP20RR021970 · NCRR · LSU HEALTH SCIENCES CENTER · PI ESTRADA, JOHN J. · 2005 to 2011
$14.1M
Prosaposin, a novel tumor marker for prostate cancerR21CA120625 · NCI · LSU HEALTH SCIENCES CENTER · PI KOOCHEKPOUR, SHAHRIAR · 2006 to 2007
$266k
NCI NIH HHS 1R21 CA120625NCRR NIH HHS 1P20 RR021970
6 · The paper itself

Abstract

backgroundFactors responsible for invasive and metastatic progression of prostate cancer (PCa) remain largely unknown. Previously, we reported cloning of prosaposin (PSAP) and its genomic amplification and/or overexpression in several androgen-independent metastatic PCa cell lines and lymph node metastases. PSAP is the lysosomal precursor of saposins, which serve as activators for lysosomal hydrolases involved in the degradation of ceramide (Cer) and other sphingolipids.

resultsOur current data show that, in metastatic PCa cells, stable down-modulation of PSAP by RNA-interference via a lysosomal proteolysis-dependent pathway decreased beta1A-integrin expression, its cell-surface clustering, and adhesion to basement membrane proteins; led to disassembly of focal adhesion complex; and decreased phosphorylative activity of focal adhesion kinase and its downstream adaptor molecule, paxillin. Cathepsin D (CathD) expression and proteolytic activity, migration, and invasion were also significantly decreased in PSAP knock-down cells. Transient-transfection studies with beta1A integrin- or CathD-siRNA oligos confirmed the cause and effect relationship between PSAP and CathD or PSAP and Cer-beta1A integrin, regulating PCa cell migration and invasion.

conclusionOur findings suggest that by a coordinated regulation of Cer levels, CathD and beta1A-integrin expression, and attenuation of "inside-out" integrin-signaling pathway, PSAP is involved in PCa invasion and therefore might be used as a molecular target for PCa therapy.

Indexed as

Cell MovementDown-RegulationBasement MembraneCathepsin DCell AdhesionCell Line, TumorCeramidesEnzyme ActivationFocal Adhesion Protein-Tyrosine KinasesFocal AdhesionsGene SilencingHumansIntegrin beta1MaleNeoplasm InvasivenessNeoplasm MetastasisCathepsin DCeramidesFocal Adhesion Protein-Tyrosine KinasesIntegrin beta1PSAP protein, humanSaposins

Identifiers

PMID20132547
PMCPMC2825248
OpenAlexW2145133052

What OpenQuestion holds

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LicenceCC BY
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.