Evidence map›Paper›PMID 18762810›Full record

ArticleOncogene2008

In vitro genetic screen identifies a cooperative role for LPA signaling and c-Myc in cell transformation.

P Taghavi, E Verhoeven, J J L Jacobs, J P Lambooij, C Stortelers, E Tanger, W H Moolenaar, M van Lohuizen

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

27 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Review
  3. Role of autotaxin in cancer stem cells.Cancer metastasis reviews · 2018
    Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Microenvironments dictating tumor cell dormancy.Recent results in cancer research. Fortschritte der Krebsforschung. Progres dans les recherches sur le cancer · 2012
    Review
  15. ERK1/2 and p38α/β signaling in tumor cell quiescence: opportunities to control dormant residual disease.Clinical cancer research : an official journal of the American Association for Cancer Research · 2011
    Review
  16. Insights into autotaxin: how to produce and present a lipid mediator.Nature reviews. Molecular cell biology · 2011
    Review
  17. Article
  18. Article
  19. Article
  20. Boronic acid-based inhibitor of autotaxin reveals rapid turnover of LPA in the circulation.Proceedings of the National Academy of Sciences of the United States of America · 2010
    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 3 institutions in 2 countries.

P TaghaviDivision of Molecular Genetics, The Netherlands Cancer Institute, Amsterdam, The Netherlands.
E Verhoeven
J J L Jacobs
J P Lambooij
C Stortelers
E Tanger
W H Moolenaar
M van Lohuizen
Oncode Institute · NLThe Netherlands Cancer Institute · NLAblynx (Belgium) · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

c-Myc drives uncontrolled cell proliferation in various human cancers. However, in mouse embryo fibroblasts (MEFs), c-Myc also induces apoptosis by activating the p19Arf tumor suppressor pathway. Tbx2, a transcriptional repressor of p19Arf, can collaborate with c-Myc by suppressing apoptosis. MEFs overexpressing c-Myc and Tbx2 are immortal but not transformed. We have performed an unbiased genetic screen, which identified 12 oncogenes that collaborate with c-Myc and Tbx2 to transform MEFs in vitro. One of them encodes the LPA2 receptor for the lipid growth factor lysophosphatidic acid (LPA). We find that LPA1 and LPA4, but not LPA3, can reproduce the transforming effect of LPA2. Using pharmacological inhibitors, we show that the in vitro cell transformation induced by LPA receptors is dependent on the Gi-linked ERK and PI3K signaling pathways. The transforming ability of LPA1, LPA2 and LPA4 was confirmed by tumor formation assays in vivo and correlated with prolonged ERK1/2 activation in response to LPA. Our results reveal a direct role for LPA receptor signaling in cell transformation and tumorigenesis in conjunction with c-Myc and reduced p19Arf expression.

Indexed as

Cell Transformation, NeoplasticGenes, mycAnimalsCell DivisionCell SurvivalCyclin-Dependent Kinase Inhibitor p16Embryo, MammalianExtracellular Signal-Regulated MAP KinasesFibroblastsGene Expression Regulation, NeoplasticGenetic TestingHumansLysophospholipidsMiceNeoplasmsReceptors, Lysophosphatidic AcidCdkn2a protein, mouseCyclin-Dependent Kinase Inhibitor p16Extracellular Signal-Regulated MAP Kinaseslysophosphatidic acidLysophospholipidsReceptors, Lysophosphatidic Acid

Identifiers

PMID18762810
OpenAlexW1966163661

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.