Evidence map›Paper›PMID 26249176›Full record

ArticleCancer research2015

Heparanase Enhances Tumor Growth and Chemoresistance by Promoting Autophagy.

Anna Shteingauz, Ilanit Boyango, Inna Naroditsky, Edward Hammond, Maayan Gruber, Ilana Doweck, Neta Ilan, Israel Vlodavsky

Abstract read
In one paragraph

Article in Cancer research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed, 2 pooled it
7.4field-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

88 citing papers in PubMed, 2 syntheses or guidelines pooled it, 160 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Circulating GLASTFrontiers in molecular biosciences · 2024
    Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. Role of heparanase in pulmonary hypertension.Frontiers in pharmacology · 2023
    Review
  19. Review
  20. Review

28 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 4 institutions in 2 countries.

Anna ShteingauzCancer and Vascular Biology Research Center, the Bruce Rappaport Faculty of Medicine, Technion, Haifa, Israel.
Ilanit BoyangoCancer and Vascular Biology Research Center, the Bruce Rappaport Faculty of Medicine, Technion, Haifa, Israel.
Inna NaroditskyDepartment of Pathology, Rambam Health Care Campus, Haifa, Israel.
Edward HammondProgen Pharmaceuticals, Brisbane, Queensland, Australia.
Maayan GruberDepartment of Otolaryngology, Head and Neck Surgery, Carmel Medical Center, Haifa, Israel.
Ilana DoweckDepartment of Otolaryngology, Head and Neck Surgery, Carmel Medical Center, Haifa, Israel.
Neta IlanCancer and Vascular Biology Research Center, the Bruce Rappaport Faculty of Medicine, Technion, Haifa, Israel.
Israel VlodavskyCancer and Vascular Biology Research Center, the Bruce Rappaport Faculty of Medicine, Technion, Haifa, Israel. Vlodavsk@mail.huji.ac.il.
Rappaport Family Institute for Research in the Medical Sciences · ILCarmel Medical Center · ILRambam Health Care Campus · ILThe University of Queensland · AU

Funding

Regulation of heparanase in cancer progressionR01CA106456 · NCI · TECHNION-ISRAEL INSTITUTE OF TECHNOLOGY · PI VLODAVSKY, ISRAEL · 2004 to 2013
$1.7M
NCI NIH HHS R01 CA106456
6 · The paper itself

Abstract

Heparanase is the only enzyme in mammals capable of cleaving heparan sulfate, an activity implicated in tumor inflammation, angiogenesis, and metastasis. Heparanase is secreted as a latent enzyme that is internalized and subjected to proteolytic processing and activation in lysosomes. Its role under normal conditions has yet to be understood. Here, we provide evidence that heparanase resides within autophagosomes, where studies in heparanase-deficient or transgenic mice established its contributions to autophagy. The protumorigenic properties of heparanase were found to be mediated, in part, by its proautophagic function, as demonstrated in tumor xenograft models of human cancer and through use of inhibitors of the lysosome (chloroquine) and heparanase (PG545), both alone and in combination. Notably, heparanase-overexpressing cells were more resistant to stress and chemotherapy in a manner associated with increased autophagy, effects that were reversed by chloroquine treatment. Collectively, our results establish a role for heparanase in modulating autophagy in normal and malignant cells, thereby conferring growth advantages under stress as well as resistance to chemotherapy. Cancer Res; 75(18); 3946-57. ©2015 AACR.

Indexed as

Amino AcidsAnimalsAntineoplastic AgentsAutophagyCarcinomaCell DivisionCell Line, TumorCells, CulturedChloroquineCisplatinDrug Resistance, NeoplasmFemaleFibroblastsGliomaGlucuronidaseHeparanaseAmino AcidsAntineoplastic AgentsChloroquineCisplatinGlucuronidaseHeparanaseMechanistic Target of Rapamycin Complex 1Membrane LipidsMultiprotein ComplexesNeoplasm ProteinsPhosphatidylethanolaminesTOR Serine-Threonine Kinases

Identifiers

PMID26249176
PMCPMC4573896
OpenAlexW2022532273

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.