Evidence map›Paper›PMID 28794411›Full record

ArticleScientific reports2017

Dextran-Catechin inhibits angiogenesis by disrupting copper homeostasis in endothelial cells.

Eugene M H Yee, Miriam B Brandl, Eddy Pasquier, Giuseppe Cirillo, Kathleen Kimpton, Maria Kavallaris, Naresh Kumar, Orazio Vittorio

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

13 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
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  11. Implications of flavonoids as potential modulators of cancer neovascularity.Journal of cancer research and clinical oncology · 2020
    Review
  12. Article
  13. Theranostics · 2018
    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

8 authors at 4 institutions in 3 countries.

Eugene M H YeeSchool of Chemistry, UNSW Australia, Sydney, NSW 2052, Australia.
Miriam B BrandlChildren's Cancer Institute, Lowy Cancer Research Centre, University of New South Wales, Sydney, Australia.
Eddy PasquierChildren's Cancer Institute, Lowy Cancer Research Centre, University of New South Wales, Sydney, Australia.
Giuseppe CirilloDepartment of Pharmacy Health and Nutritional Science University of Calabria Arcavacata di Rende, Rende, Italy.ORCID 0000-0002-9592-1333
Kathleen KimptonChildren's Cancer Institute, Lowy Cancer Research Centre, University of New South Wales, Sydney, Australia.
Maria KavallarisChildren's Cancer Institute, Lowy Cancer Research Centre, University of New South Wales, Sydney, Australia.
Naresh KumarSchool of Chemistry, UNSW Australia, Sydney, NSW 2052, Australia.
Orazio VittorioChildren's Cancer Institute, Lowy Cancer Research Centre, University of New South Wales, Sydney, Australia. OVittorio@ccia.org.au.
UNSW Sydney · AUAix-Marseille Université · FRUniversity of Calabria · ITUniversity of Technology Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Formation of blood vessels, or angiogenesis, is crucial to cancer progression. Thus, inhibiting angiogenesis can limit the growth and spread of tumors. The natural polyphenol catechin has moderate anti-tumor activity and interacts with copper, which is essential for angiogenesis. Catechin is easily metabolized in the body and this limits its clinical application. We have recently shown that conjugation of catechin with dextran (Dextran-Catechin) improves its serum stability, and exhibits potent anti-tumor activity against neuroblastoma by targeting copper homeostasis. Herein, we investigated the antiangiogenic activity of Dextran-Catechin and its mechanism. We found that Dextran-Catechin displayed potent antiangiogenic activity in vitro and in vivo. We demonstrated Dextran-Catechin generates reactive oxygen species which in turns disrupts copper homeostasis by depleting the copper importer CTR-1 and copper trafficking ATOX-1 protein. Mechanistically, we showed that disrupting copper homeostasis by knockdown of either CTR-1 or ATOX-1 protein can inhibit angiogenesis in endothelial cells. This data strongly suggests the Dextran-Catechin potent antiangiogenic activity is mediated by disrupting copper homeostasis. Thus, compounds such as Dextran-Catechin that affects both tumor growth and angiogenesis could lead the way for development of new drugs against high copper levels tumors.

Indexed as

Neovascularization, PathologicAnimalsAntineoplastic AgentsCatechinCation Transport ProteinsCells, CulturedCell SurvivalCopperCopper Transporter 1Copper Transport ProteinsDextransDisease Models, AnimalEndothelial CellsHeterograftsHomeostasisHumansAntineoplastic AgentsATOX1 protein, humanCatechinCation Transport ProteinsCopperCopper Transporter 1Copper Transport ProteinsDextransMetallochaperonesMolecular ChaperonesReactive Oxygen SpeciesSLC31A1 protein, humanTrace Elements

Identifiers

PMID28794411
PMCPMC5550437
OpenAlexW2744515512

What OpenQuestion holds

Textmetadata
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.