Evidence map›Paper›PMID 28147305›Full record

ArticleNeoplasia (New York, N.Y.)2017

The Heparanase Inhibitor PG545 Attenuates Colon Cancer Initiation and Growth, Associating with Increased p21 Expression.

Preeti Singh, Alexandra Blatt, Sari Feld, Yaniv Zohar, Esraa Saadi, Liza Barki-Harrington, Edward Hammond, Neta Ilan, Israel Vlodavsky, Yehuda Chowers and 1 more

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

16 citing papers in PubMed, 25 citations in OpenAlex.

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  6. The Heparanase Regulatory Network in Health and Disease.International journal of molecular sciences · 2021
    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

11 authors at 2 institutions in 1 country.

Preeti SinghCancer and Vascular Biology Research Center, the Bruce Rappaport Faculty of Medicine, Technion, Haifa 31096, Israel.
Alexandra BlattDepartment of Gastroenterology, Rambam Health Care Campus and Bruce Rappaport School of Medicine, Technion, Haifa 3109601, Israel.
Sari FeldCancer and Vascular Biology Research Center, the Bruce Rappaport Faculty of Medicine, Technion, Haifa 31096, Israel.
Yaniv ZoharDepartment of Pathology, Rambam Health Care Campus and Bruce Rappaport School of Medicine, Technion, Haifa 3109601, Israel.
Esraa SaadiDepartment of Human Biology, University of Haifa, Haifa 31905, Israel.
Liza Barki-HarringtonDepartment of Human Biology, University of Haifa, Haifa 31905, Israel.
Edward HammondZucero Therapeutics, Darra, QLD 4076, Australia.
Neta IlanCancer and Vascular Biology Research Center, the Bruce Rappaport Faculty of Medicine, Technion, Haifa 31096, Israel.
Israel VlodavskyCancer and Vascular Biology Research Center, the Bruce Rappaport Faculty of Medicine, Technion, Haifa 31096, Israel.
Yehuda ChowersDepartment of Gastroenterology, Rambam Health Care Campus and Bruce Rappaport School of Medicine, Technion, Haifa 3109601, Israel. Electronic address: y_chowers@rambam.health.gov.il.
Elizabeth HalfDepartment of Gastroenterology, Rambam Health Care Campus and Bruce Rappaport School of Medicine, Technion, Haifa 3109601, Israel. Electronic address: E_Half@rambam.health.gov.il.
Rambam Health Care Campus · ILUniversity of Haifa · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Heparanase activity is highly implicated in cellular invasion and tumor metastasis, a consequence of cleavage of heparan sulfate and remodeling of the extracellular matrix underlying epithelial and endothelial cells. Heparanase expression is rare in normal epithelia, but is often induced in tumors, associated with increased tumor metastasis and poor prognosis. In addition, heparanase induction promotes tumor growth, but the molecular mechanism that underlines tumor expansion by heparanase is still incompletely understood. Here, we provide evidence that heparanase down regulates the expression of p21 (WAF1/CIP1), a cyclin-dependent kinase inhibitor that attenuates the cell cycle. Notably, a reciprocal effect was noted for PG545, a potent heparanase inhibitor. This compound efficiently reduced cell proliferation, colony formation, and tumor xenograft growth, associating with a marked increase in p21 expression. Utilizing the APC Min

Indexed as

AnimalsCell Cycle CheckpointsCell Line, TumorCell ProliferationCell Transformation, NeoplasticColonic NeoplasmsColonic PolypsCyclin-Dependent Kinase Inhibitor p21Disease Models, AnimalDown-RegulationEnzyme ActivationGene Expression Regulation, NeoplasticGlucuronidaseHeparanaseHumansMiceCyclin-Dependent Kinase Inhibitor p21GlucuronidaseHeparanaseNF-kappa BPG 545SaponinsToll-Like Receptors

Identifiers

PMID28147305
PMCPMC5279702
OpenAlexW2582024022

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.