Evidence map›Paper›PMID 17334389›Full record

ArticleOncogene2007

Opposing roles of netrin-1 and the dependence receptor DCC in cancer cell invasion, tumor growth and metastasis.

S Rodrigues, O De Wever, E Bruyneel, R J Rooney, C Gespach

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

57 citing papers in PubMed, 97 citations in OpenAlex.

  1. Article
  2. Research progress of the netrins and their receptors in cancer.Journal of cellular and molecular medicine · 2024
    Review
  3. Article
  4. Article
  5. Article
  6. International journal of biological sciences · 2022
    Article
  7. Article
  8. Review
  9. Article
  10. Serum netrin-1 as a biomarker for colorectal cancer detection.Cancer biomarkers : section A of Disease markers · 2020
    Article
  11. Review
  12. AInternational journal of molecular sciences · 2019
    Review
  13. Article
  14. Article
  15. The role ofAnnals of translational medicine · 2018
    Review
  16. Breaking down barriers: the evolution of cell invasion.Current opinion in genetics & development · 2017
    Review
  17. Article
  18. Microbial carcinogenic toxins and dietary anti-cancer protectants.Cellular and molecular life sciences : CMLS · 2017
    Review
  19. Article
  20. 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

5 authors at 4 institutions in 3 countries.

S RodriguesINSERM, U673, Paris, France.
O De Wever
E Bruyneel
R J Rooney
C Gespach
Inserm · FRGhent University Hospital · BEHuman Genome Sciences (United States) · USSorbonne Université · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Deleted in colon cancer (DCC) and UNC5 function as netrin dependence receptors by inducing apoptosis in the absence of their ligand and accordingly were recently designated as putative conditional tumor suppressors. Herein, we determined whether netrin-1 and its receptors are implicated in cancer cell invasion and tumor progression. Expression of DCC, UNC5 and adenosine A2B-receptors (A2B-Rs) was investigated by reverse transcription polymerase chain reaction in human colon cancer cells. The impact of DCC restitution and netrin-1 was evaluated on collagen type I invasion, tumor growth and metastasis in nude mice, cancer cell survival and gene expression profiling. Flow cytometry, poly(ADP-ribose)polymerase-1 and caspase-8 activation were used to evaluate the impact of DCC on cell death. Both netrin-1 and A2B-R activation induced the invasive phenotype through the Rho-Rho kinase axis in DCC-deficient human colorectal cancer cells. Restitution of wild-type DCC blocked invasion induced by netrin-1, A2B-R agonist and other agents. Ectopic expression of netrin-1 led to increased growth of human colon tumor xenografts in athymic mice. Conversely, introduction of wt-DCC in kidney MDCKts.src-ggl cells strongly inhibited metastasis in lymph nodes and lungs and increased sensitivity to apoptosis in hypoxia. DNA microarrays revealed that netrin and DCC had common and divergent impacts on gene expression linked to cell cycle, survival, surface signaling and adhesion. Our findings underscore that netrin is a potent invasion and tumor growth-promoting agent and that DCC is a metastasis suppressor gene targeting both proinvasive and survival pathways in a cumulative manner.

Indexed as

AnimalsBlotting, WesternCell HypoxiaCell Line, TransformedCell Line, TumorCell MovementCell ProliferationCell SurvivalDCC ReceptorGene Expression Regulation, NeoplasticHT29 CellsHumansMiceMice, NudeNeoplasm InvasivenessNeoplasm MetastasisDCC protein, humanDCC ReceptorNerve Growth FactorsNetrin-1NTN1 protein, humanNtn1 protein, mouseReceptor, Adenosine A2BReceptors, Cell SurfaceTumor Suppressor Proteins

Identifiers

PMID17334389
OpenAlexW2088064365

What OpenQuestion holds

Textmetadata
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.