Evidence map›Paper›PMID 24293316›Full record

ArticleEMBO molecular medicine2013

Combining chemotherapeutic agents and netrin-1 interference potentiates cancer cell death.

Andrea Paradisi, Marion Creveaux, Benjamin Gibert, Guillaume Devailly, Emeline Redoulez, David Neves, Elsa Cleyssac, Isabelle Treilleux, Christian Klein, Gerhard Niederfellner and 3 more

Open access · goldAbstract read
In one paragraph

Article in EMBO molecular medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

34 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Research progress of the netrins and their receptors in cancer.Journal of cellular and molecular medicine · 2024
    Review
  7. Genes · 2024
    Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Δ40p53 isoform up-regulates netrin-1/UNC5B expression and potentiates netrin-1 pro-oncogenic activity.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  18. Review
  19. Article
  20. Cancers · 2020
    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

13 authors at 6 institutions in 2 countries.

Andrea ParadisiApoptosis, Cancer and Development Laboratory - Equipe labellisée 'La Ligue', LabEx DEVweCAN, Centre de Cancérologie de Lyon, INSERM U1052-CNRS UMR5286, Université de Lyon, Centre Léon Bérard, Lyon, France.
Marion Creveaux
Benjamin Gibert
Guillaume Devailly
Emeline Redoulez
David Neves
Elsa Cleyssac
Isabelle Treilleux
Christian Klein
Gerhard Niederfellner
Philippe A Cassier
Agnès Bernet
Patrick Mehlen
Université Claude Bernard Lyon 1 · FRNetris Pharma (France) · FRInserm · FRRoche Pharma AG (Germany) · DECentre Léon Bérard · FRCentre National de la Recherche Scientifique · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The secreted factor netrin-1 is upregulated in a fraction of human cancers as a mechanism to block apoptosis induced by netrin-1 dependence receptors DCC and UNC5H. Targeted therapies aiming to trigger tumour cell death via netrin-1/receptors interaction interference are under preclinical evaluation. We show here that Doxorubicin, 5-Fluorouracil, Paclitaxel and Cisplatin treatments trigger, in various human cancer cell lines, an increase of netrin-1 expression which is accompanied by netrin-1 receptors increase. This netrin-1 upregulation which appears to be p53-dependent is a survival mechanism as netrin-1 silencing by siRNA is associated with a potentiation of cancer cell death upon Doxorubicin treatment. We show that candidate drugs interfering with netrin-1/netrin-1 receptors interactions potentiate Doxorubicin, Cisplatin or 5-Fluorouracil-induced cancer cell death in vitro. Moreover, in a model of xenografted nude mice, we show that systemic Doxorubicin treatment triggers netrin-1 upregulation in the tumour but not in normal organs, enhancing and prolonging tumour growth inhibiting effect of a netrin-1 interfering drug. Together these data suggest that combining conventional chemotherapies with netrin-1 interference could be a promising therapeutic approach.

Indexed as

AnimalsAntineoplastic AgentsApoptosisCell Line, TumorCisplatinDoxorubicinFemaleFluorouracilHumansLung NeoplasmsMiceMice, NudeNerve Growth FactorsNetrin-1Netrin ReceptorsReceptors, Cell SurfaceAntineoplastic AgentsCisplatinDoxorubicinFluorouracilNerve Growth FactorsNetrin-1Netrin ReceptorsNTN1 protein, humanNtn1 protein, mouseReceptors, Cell SurfaceRNA, Small InterferingTumor Suppressor Protein p53Tumor Suppressor ProteinsUNC5B protein, humancancer therapyDCCdependence receptornetrin-1, p53

Identifiers

PMID24293316
PMCPMC3914534
OpenAlexW2158172740

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.