Evidence map›Paper›PMID 27419371›Full record

ArticleOncotarget2017

Antitumor activity of sulfated hyaluronic acid fragments in pre-clinical models of bladder cancer.

Andre R Jordan, Soum D Lokeshwar, Luis E Lopez, Martin Hennig, Juan Chipollini, Travis Yates, Marie C Hupe, Axel S Merseburger, Aviva Shiedlin, Wolfgang H Cerwinka and 2 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

15 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. The Roles of Glycans in Bladder Cancer.Frontiers in oncology · 2020
    Review
  13. Article
  14. Article
  15. Article
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

12 authors at 4 institutions in 2 countries.

Andre R JordanSheila and David Fuente Graduate Program in Cancer Biology, Sylvester Comprehensive Cancer Center, University of Miami-Miller School of Medicine, Miami, FL, USA.
Soum D LokeshwarHonors Program in Medical Education, University of Miami-Miller School of Medicine, Miami, FL, USA.
Luis E LopezDepartment of Biochemistry and Molecular Biology, Medical College of Georgia, Augusta University, Augusta, GA, USA.
Martin HennigDepartment of Biochemistry and Molecular Biology, Medical College of Georgia, Augusta University, Augusta, GA, USA.
Juan ChipolliniDepartment of Urology, University of Miami-Miller School of Medicine, Miami, FL, USA.
Travis YatesSheila and David Fuente Graduate Program in Cancer Biology, Sylvester Comprehensive Cancer Center, University of Miami-Miller School of Medicine, Miami, FL, USA.
Marie C HupeDepartment of Biochemistry and Molecular Biology, Medical College of Georgia, Augusta University, Augusta, GA, USA.
Axel S MerseburgerDepartment of Urology, University of Lübeck, Lübeck, Germany.
Aviva ShiedlinDrug and Biomaterial R&D, Genzyme Corporation, Cambridge, MA, USA.
Wolfgang H CerwinkaDepartment of Urology, University of Miami-Miller School of Medicine, Miami, FL, USA.
Kebin LiuDepartment of Biochemistry and Molecular Biology, Medical College of Georgia, Augusta University, Augusta, GA, USA.
Vinata B LokeshwarDepartment of Biochemistry and Molecular Biology, Medical College of Georgia, Augusta University, Augusta, GA, USA.
Augusta University · USUniversity of Miami · USSylvester Comprehensive Cancer Center · USUniversity of Lübeck · DE

Funding

SUPPLEMENT FOR MARC SCIENTIFIC COMMUNICATIONS TECHNOLOGYT34GM008078 · NIGMS · BROOKLYN COLLEGE · PI HAINLINE, LOUISE, RABIN, LAURA A. · 1985 to 2022
$8.2M
Role of IRF8 in Tumor Rejection and SuppressionR01CA133085 · NCI · AUGUSTA UNIVERSITY · PI LIU, KEBIN · 2008 to 2019
$2.9M
Mechanisms of Bladder Cancer ProgressionR01CA072821 · NCI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI LOKESHWAR, VINATA B · 2003 to 2014
$2.4M
Novel Biomarkers for the Clinical Management of Bladder CancerR01CA227277 · NCI · AUGUSTA UNIVERSITY · PI LOKESHWAR, VINATA B · 2018 to 2023
$2.2M
Dietary Combination For Prevention of Metastatic Renal Cell CarcinomaR01CA176691 · NCI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI LOKESHWAR, VINATA B · 2014 to 2019
$1.7M
Role of CYP3A4 in Prostate CancerR21CA184018 · NCI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI LOKESHWAR, VINATA B · 2014 to 2015
$367k
Role of SLC13A3 in Renal Cell CarcinomaF31CA210612 · NCI · AUGUSTA UNIVERSITY · PI JORDAN, ANDRE R · 2016 to 2018
$102k
NCI NIH HHS F31 CA210612NCI NIH HHS R01 CA072821NCI NIH HHS R01 CA133085NCI NIH HHS R01 CA176691NCI NIH HHS R01 CA227277NCI NIH HHS R21 CA184018
6 · The paper itself

Abstract

Tumor cell-derived hyaluronidase HYAL-1 degrades hyaluronic acid (HA) into angiogenic fragments (AGF: 10-12 disaccharides). AGF support tumor growth and progression. Urine and tissue HAase/HYAL-1 levels are sensitive markers for high-grade bladder cancer (BCa) and its metastasis. In preclinical models of BCa, we evaluated whether o-sulfated AGF (sHA-F) inhibits HAase activity and has antitumor activity. At IC50 for HAase activity inhibition (5-20 μg/ml [0.4-1.7 μM]), sHA-F significantly inhibited proliferation, motility and invasion of HYAL-1 expressing BCa cells (253J-Lung, HT1376, UMUC-3), P<0.001. sHA-F did not affect the growth of HYAL-1 non-expressing BCa (5637, RT4, T24, TCCSUP) and normal urothelial (Urotsa, SV-HUC1) cells. sHA-F treatment induced apoptosis by death receptor pathway. sHA-F downregulated transcript and/or protein levels of HA receptors (CD44, RHAMM), p-AKT, β-catenin, pβ-Catenin(S552), Snail and Twist but increased levels of pβ-Catenin(T41/S45), pGSK-3α/β(S21/S9) and E-cadherin. sHA-F also inhibited CD44/Phosphoinositide 3-kinase (PI-3K) complex formation and PI-3K activity. AGF addition or myristoylated-AKT overexpression attenuated sHA-F effects. Contrarily, HYAL-1 expression sensitized RT4 cells to sHA-F treatment. In the 253J-L and HT1376 xenograft models, sHA-F treatment significantly inhibited tumor growth (P<0.001), plausibly by inhibiting angiogenesis and HA receptor-PI-3K/AKT signaling. This study delineates that sHA-F targets tumor-associated HA-HAase system and could be potentially useful in BCa treatment.

Indexed as

AnimalsAntineoplastic AgentsApoptosisCell Line, TumorCell MovementCell ProliferationDisease Models, AnimalDrug Evaluation, PreclinicalHumansHyaluronic AcidMicePhosphatidylinositol 3-KinasesUrinary Bladder NeoplasmsXenograft Model Antitumor AssaysAntineoplastic AgentsHyaluronic AcidPhosphatidylinositol 3-Kinasesbladder cancerhyaluronic acidhyaluronidasesulfated-HAtargeted therapy

Identifiers

PMID27419371
PMCPMC5421845
OpenAlexW2464093984

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.