Evidence map›Paper›PMID 22954454›Full record

ReviewBiochimica et biophysica acta2013

Role of the autotaxin-lysophosphatidate axis in cancer resistance to chemotherapy and radiotherapy.

David N Brindley, Fang-Tsyr Lin, Gabor J Tigyi

Registry-linked trialOpen access · greenAbstract readReview
In one paragraph

Review in Biochimica et biophysica acta, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03115866 (FRUVEDomics Study), which is not on this map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
3.9field-weighted citation impact, top 6% 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.

NCT03115866 nacompletednot on this mapstarted 2015, after this paper: background citation

FRUVEDomics Study: Use of a Behavioral Nutrition Intervention in Young Adults to Identify Modifiable Metabolomics and Microbiome Risk

TypeinterventionalSponsorWest Virginia UniversityRan2015 to 2019Enrolled53ConditionsMetabolic SyndromeArmsFRUVEDomics
3 · Its place in the literature

Who cites it

70 citing papers in PubMed, 118 citations in OpenAlex.

  1. Trial
  2. Review
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  6. Review
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  11. World journal of gastrointestinal oncology · 2022
    Review
  12. Article
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  15. Review
  16. Review
  17. Review
  18. Therapeutic Strategies for Targeting Ovarian Cancer Stem Cells.International journal of molecular sciences · 2021
    Review
  19. Review
  20. Article

10 more citing papers are in PubMed but not listed here.

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

3 authors at 3 institutions in 2 countries.

David N BrindleyDepartment of Biochemistry, University of Alberta, Edmonton, Alberta, Canada. david.brindley@ualberta.ca
Fang-Tsyr Lin
Gabor J Tigyi
Baylor College of Medicine · USUniversity of Alberta · CAUniversity of Tennessee Health Science Center · US

Funding

Ligand Recognition by Phospholipid Growth Factor ReceptorsR01CA092160 · NCI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI TIGYI, GABOR J · 2001 to 2022
$5.9M
Analysis of Radiomitigative Cell SignalingR01AI080405 · NIAID · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI TIGYI, GABOR J · 2008 to 2012
$2.1M
Novel Radiomitigators Targeting LPA ReceptorsI01BX001187 · VA · MEMPHIS VA MEDICAL CENTER · PI TIGYI, GABOR J · 2013 to 2016
–
BLRD VA I01 BX001187CIHRNCI NIH HHS CA92160NCI NIH HHS R01 CA092160NIAID NIH HHS AI80405NIAID NIH HHS R01 AI080405
6 · The paper itself

Abstract

High expression of autotaxin in cancers is often associated with increased tumor progression, angiogenesis and metastasis. This is explained mainly since autotaxin produces the lipid growth factor, lysophosphatidate (LPA), which stimulates cell division, survival and migration. It has recently become evident that these signaling effects of LPA also produce resistance to chemotherapy and radiation-induced cell death. This results especially from the stimulation of LPA(2) receptors, which depletes the cell of Siva-1, a pro-apoptotic signaling protein and stimulates prosurvival kinase pathways through a mechanism mediated via TRIP-6. LPA signaling also increases the formation of sphingosine 1-phosphate, a pro-survival lipid. At the same time, LPA decreases the accumulation of ceramides, which are used in radiation therapy and by many chemotherapeutic agents to stimulate apoptosis. The signaling actions of extracellular LPA are terminated by its dephosphorylation by a family of lipid phosphate phosphatases (LPP) that act as ecto-enzymes. In addition, lipid phosphate phoshatase-1 attenuates signaling downstream of the activation of both LPA receptors and receptor tyrosine kinases. This makes many cancer cells hypersensitive to the action of various growth factors since they often express low LPP1/3 activity. Increasing our understanding of the complicated signaling pathways that are used by LPA to stimulate cell survival should identify new therapeutic targets that can be exploited to increase the efficacy of chemo- and radio-therapy. This article is part of a Special Issue entitled Advances in Lysophospholipid Research.

Indexed as

Drug Resistance, NeoplasmRadiation ToleranceAnimalsHumansLysophospholipase DLysophospholipidsNeoplasmsPhosphoric Diester HydrolasesReceptors, Lysophosphatidic AcidSignal Transductionlysophosphatidic acidLysophospholipase DLysophospholipidsPhosphoric Diester HydrolasesReceptors, Lysophosphatidic Acid

Identifiers

PMID22954454
PMCPMC3584168
OpenAlexW2039346157

What OpenQuestion holds

Textmetadata
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Read underepoch 390

Registered trials

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.