Evidence map›Paper›PMID 27543953›Full record

ArticleInternational journal of cancer2016

Heparan sulfate proteoglycans mediate renal carcinoma metastasis.

Henry Qazi, Zhong-Dong Shi, Jonathan W Song, Limary M Cancel, Peigen Huang, Ye Zeng, Sylvie Roberge, Lance L Munn, John M Tarbell

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
–field-weighted citation impact
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

26 citing papers in PubMed.

  1. Tumor Metastasis in the Microcirculation.Advances in experimental medicine and biology · 2026
    Review
  2. Migrasomes in cancers: from the biogenesis mechanism to therapeutic implications.Extracellular vesicles and circulating nucleic acids · 2026
    Review
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  19. Biogenesis of Extracellular Vesicles.Sub-cellular biochemistry · 2021
    Article
  20. Review
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

9 authors.

Henry QaziWallace H. Coulter Laboratory, Department of Biomedical Engineering, The City College of New York, The City University of New York, New York, NY 10032, USA.
Zhong-Dong ShiDevelopmental Biology Program, Sloan-Kettering Institute, New York, NY 10065, USA.
Jonathan W SongComprehensive Cancer Center, Department of Mechanical and Aerospace Engineering, The Ohio State University, Columbus, OH 43210, USA.
Limary M CancelWallace H. Coulter Laboratory, Department of Biomedical Engineering, The City College of New York, The City University of New York, New York, NY 10032, USA.
Peigen HuangEdwin L. Steele Laboratories for Tumor Biology, Department of Radiation Oncology, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA 02129, USA.
Ye ZengWallace H. Coulter Laboratory, Department of Biomedical Engineering, The City College of New York, The City University of New York, New York, NY 10032, USA.
Sylvie RobergeEdwin L. Steele Laboratories for Tumor Biology, Department of Radiation Oncology, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA 02129, USA.
Lance L MunnEdwin L. Steele Laboratories for Tumor Biology, Department of Radiation Oncology, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA 02129, USA. tarbell@ccny.cuny.edu.
John M TarbellWallace H. Coulter Laboratory, Department of Biomedical Engineering, The City College of New York, The City University of New York, New York, NY 10032, USA. lmunn@mgh.harvard.edu.

Funding

Targeting glycocalyx-mediated mechanisms of tumor metastasisR01CA204949 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI MUNN, LANCE L., TARBELL, JOHN M · 2017 to 2021
$2.3M
NCI NIH HHS R01 CA204949
6 · The paper itself

Abstract

The surface proteoglycan/glycoprotein layer (glycocalyx) on tumor cells has been associated with cellular functions that can potentially enable invasion and metastasis. In addition, aggressive tumor cells with high metastatic potential have enhanced invasion rates in response to interstitial flow stimuli in vitro. Our previous studies suggest that heparan sulfate (HS) in the glycocalyx plays an important role in this flow mediated mechanostransduction and upregulation of invasive and metastatic potential. In this study, highly metastatic renal cell carcinoma cells were genetically modified to suppress HS production by knocking down its synthetic enzyme NDST1. Using modified Boyden chamber and microfluidic assays, we show that flow-enhanced invasion is suppressed in HS deficient cells. To assess the ability of these cells to metastasize in vivo, parental or knockdown cells expressing fluorescence reporters were injected into kidney capsules in SCID mice. Histological analysis confirmed that there was a large reduction (95%) in metastasis to distant organs by tumors formed from the NDST1 knockdown cells compared to control cells with intact HS. The ability of these cells to invade surrounding tissue was also impaired. The substantial inhibition of metastasis and invasion upon reduction of HS suggests an active role for the tumor cell glycocalyx in tumor progression.

Indexed as

AnimalsCarcinoma, Renal CellCell Line, TumorCell MovementDisease Models, AnimalGene ExpressionGene Knockout TechniquesHeparan Sulfate ProteoglycansHumansKidney NeoplasmsMaleMiceMice, SCIDNeoplasm MetastasisPhenotypeRNA InterferenceHeparan Sulfate Proteoglycansheparitin sulfotransferaseRNA, Small InterferingSulfotransferasesglycocalyxinterstitial flowmechanobiologymetastasisNDST1

Identifiers

PMID27543953
PMCPMC7718768

What OpenQuestion holds

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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.