Evidence map›Paper›PMID 20840586›Full record

ReviewThe FEBS journal2010

Proteoglycans in health and disease: new concepts for heparanase function in tumor progression and metastasis.

Uri Barash, Victoria Cohen-Kaplan, Ilana Dowek, Ralph D Sanderson, Neta Ilan, Israel Vlodavsky

Abstract readReview
In one paragraph

Review in The FEBS journal, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
100citing papers in PubMed, 1 pooled it
8.4field-weighted citation impact, top 2% 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

100 citing papers in PubMed, 1 synthesis or guideline pooled it, 170 citations in OpenAlex.

  1. Pooled it
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  15. Heparanase modulation by Wingless/INT (Wnt).Molecular biology reports · 2021
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40 more citing papers are in PubMed but not listed here.

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

6 authors at 3 institutions in 2 countries.

Uri BarashCancer and Vascular Biology Research Center, Rappaport Faculty of Medicine, Haifa, Israel.
Victoria Cohen-Kaplan
Ilana Dowek
Ralph D Sanderson
Neta Ilan
Israel Vlodavsky
Rappaport Family Institute for Research in the Medical Sciences · ILCarmel Medical Center · ILUniversity of Alabama at Birmingham · US

Funding

Heparanase Regulation of Myeloma Metastasis: Mechanism and TherapyR01CA138340 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI SANDERSON, RALPH D · 2009 to 2018
$3.3M
Novel Heparanase Inhibitors for Cancer TherapyR01CA138535 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI SANDERSON, RALPH D · 2010 to 2014
$1.8M
Regulation of heparanase in cancer progressionR01CA106456 · NCI · TECHNION-ISRAEL INSTITUTE OF TECHNOLOGY · PI VLODAVSKY, ISRAEL · 2004 to 2013
$1.7M
NCI NIH HHS CA106456NCI NIH HHS CA138535NCI NIH HHS R01 CA106456NCI NIH HHS R01 CA138340NCI NIH HHS R01 CA138535
6 · The paper itself

Abstract

Heparanase is an endo-β-D-glucuronidase capable of cleaving heparan sulfate side chains at a limited number of sites, yielding heparan sulfate fragments of still appreciable size. Importantly, heparanase activity correlates with the metastatic potential of tumor-derived cells, attributed to enhanced cell dissemination as a consequence of heparan sulfate cleavage and remodeling of the extracellular matrix and basement membrane underlying epithelial and endothelial cells. Similarly, heparanase activity is implicated in neovascularization, inflammation and autoimmunity, involving the migration of vascular endothelial cells and activated cells of the immune system. The cloning of a single human heparanase cDNA 10 years ago enabled researchers to critically approve the notion that heparan sulfate cleavage by heparanase is required for structural remodeling of the extracellular matrix, thereby facilitating cell invasion. Progress in the field has expanded the scope of heparanase function and its significance in tumor progression and other pathologies. Notably, although heparanase inhibitors attenuated tumor progression and metastasis in several experimental systems, other studies revealed that heparanase also functions in an enzymatic activity-independent manner. Thus, inactive heparanase was noted to facilitate adhesion and migration of primary endothelial cells and to promote phosphorylation of signaling molecules such as Akt and Src, facilitating gene transcription (i.e. vascular endothelial growth factor) and phosphorylation of selected Src substrates (i.e. endothelial growth factor receptor). The concept of enzymatic activity-independent function of heparanase gained substantial support by the recent identification of the heparanase C-terminus domain as the molecular determinant behind its signaling capacity. Identification and characterization of a human heparanase splice variant (T5) devoid of enzymatic activity and endowed with protumorigenic characteristics, elucidation of cross-talk between heparanase and other extracellular matrix-degrading enzymes, and identification of single nucleotide polymorphism associated with heparanase expression and increased risk of graft versus host disease add other layers of complexity to heparanase function in health and disease.

Indexed as

Antineoplastic AgentsDisease ProgressionEnzyme InhibitorsErbB ReceptorsGlucuronidaseHead and Neck NeoplasmsHeparanaseHeparan SulfateHumansMultiple MyelomaNeoplasm MetastasisNeoplasmsProteoglycansSignal TransductionAntineoplastic AgentsEnzyme InhibitorsErbB ReceptorsGlucuronidaseHeparanaseHeparan SulfateProteoglycans

Identifiers

PMID20840586
PMCPMC3000436
OpenAlexW1502893100

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.