Evidence map›Paper›PMID 14691447›Full record

ArticleOncogene2004

Microarray analysis identifies Autotaxin, a tumour cell motility and angiogenic factor with lysophospholipase D activity, as a specific target of cell transformation by v-Jun.

Elizabeth J Black, Timothy Clair, Jeffrey Delrow, Paul Neiman, David A F Gillespie

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2004. 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
2.1field-weighted citation impact, top 13% 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, 64 citations in OpenAlex.

  1. Review
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  12. Autotaxin-lysophosphatidic acid signaling axis mediates tumorigenesis and development of acquired resistance to sunitinib in renal cell carcinoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2013
    Article
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  16. Review
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  19. ATX-LPA receptor axis in inflammation and cancer.Cell cycle (Georgetown, Tex.) · 2009
    Review
  20. Autotaxin.Cellular and molecular life sciences : CMLS · 2009
    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

5 authors at 4 institutions in 2 countries.

Elizabeth J BlackBeatson Institute for Cancer Research, Cancer Research Campaign Beatson Laboratories, Garscube Estate, Switchback Road, Bearsden, Glasgow G61 1BD, UK.
Timothy Clair
Jeffrey Delrow
Paul Neiman
David A F Gillespie
Fred Hutch Cancer Center · USCancer Research UK Scotland Institute · GBNational Cancer Institute · USUniversity of Glasgow · GB

Funding

MOLECULAR MECHANISMS IN NEOPLASIAR01CA020068 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI NEIMAN, PAUL ERIC · 1985 to 2008
$2.6M
NCI NIH HHS R01 CA20068
6 · The paper itself

Abstract

We have used chicken cDNA microarrays to investigate gene-expression changes induced during transformation of chick embryo fibroblasts (CEF) by the viral Jun oncoprotein encoded by ASV17. This analysis reveals that v-Jun induces increases and decreases of varying magnitude in the expression of genes involved in diverse cellular functions, most of which have not been detected in previous screens for putative v-Jun targets. In all, 27 individual genes were identified, whose expression is increased threefold or more in v-Jun-transformed cells, including genes involved in energy generation, protein synthesis, and gene transcription. Interestingly, this group includes the hypoxia-inducible factor-1 alpha (Hif-1alpha) transcription factor and the glycolytic enzyme enolase, suggesting that adaptation to hypoxia could play a role in tumorigenesis by v-Jun. We also identified 32 genes whose expression is decreased threefold or more, including chaperones, components of the cytoskeleton, and, unexpectedly, DNA replication factors. The gene whose expression is upregulated most dramatically (approximately 100-fold) encodes Autotaxin (ATX), a secreted tumor motility-promoting factor with lysophospholipase D activity. Strikingly, v-Jun-transformed CEF secrete catalytically active ATX and chemotactic activity, which can be detected in conditioned medium. ATX is not detectably expressed in normal CEF or CEF transformed by the v-Src or v-Myc oncoproteins, indicating that induction of this putative autocrine/paracrine factor is a specific consequence of cell transformation by v-Jun. ATX has been implicated in both angiogenesis and invasion, and could therefore play an important role in tumorigenesis by v-Jun in vivo.

Indexed as

Multienzyme ComplexesAnimalsCell Transformation, NeoplasticChick EmbryoDown-RegulationGlucose-6-Phosphate IsomeraseGlycoproteinsLysophospholipase DOligonucleotide Array Sequence AnalysisOncogene Protein p65(gag-jun)Phosphodiesterase IPhosphoric Diester HydrolasesPyrophosphatasesUp-RegulationGlucose-6-Phosphate IsomeraseGlycoproteinsLysophospholipase DMultienzyme ComplexesOncogene Protein p65(gag-jun)Phosphodiesterase IPhosphoric Diester HydrolasesPyrophosphatases

Identifiers

PMID14691447
OpenAlexW2039173160

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.