Evidence map›Paper›PMID 28255537›Full record

ArticleFEBS open bio2016

The molecular mechanism by which saturated lysophosphatidylcholine attenuates the metastatic capacity of melanoma cells.

Thomas Ross, Bastian Jakubzig, Manuel Grundmann, Ulrich Massing, Evi Kostenis, Martin Schlesinger, Gerd Bendas

Open access · goldAbstract read
In one paragraph

Article in FEBS open bio, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.2field-weighted citation impact, top 19% 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

22 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Article
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  4. The role of phosphatidylcholine metabolism in tumors.Medical oncology (Northwood, London, England) · 2025
    Review
  5. Article
  6. Article
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  8. Review
  9. Characterization of Lipid Alterations by OncogenicOmics : a journal of integrative biology · 2023
    Article
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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

7 authors at 2 institutions in 1 country.

Thomas RossDepartment of Pharmaceutical Chemistry II University of Bonn Germany.
Bastian JakubzigDepartment of Pharmaceutical Chemistry II University of Bonn Germany.
Manuel GrundmannDepartment of Pharmaceutical Biology University of Bonn Germany.
Ulrich MassingAndreas Hettich GmbH & Co. KGF&E Lifescience Applications Freiburg Germany; Faculty of Chemistry & Pharmacy University of Freiburg Germany.
Evi KostenisDepartment of Pharmaceutical Biology University of Bonn Germany.
Martin SchlesingerDepartment of Pharmaceutical Chemistry II University of Bonn Germany.
Gerd BendasDepartment of Pharmaceutical Chemistry II University of Bonn Germany.
University of Bonn · DEUniversity of Freiburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lysophophatidylcholine (LysoPC) is an abundant constituent in human plasma. Patients with malignant cancer diseases have attenuated LysoPC plasma levels, and thus LysoPC has been examined as a metabolic biomarker for cancer prediction. Preclinical studies have shown that solid tumor cells drastically degrade LysoPCs by incorporating their free fatty acids into cell membrane phospholipids. In this way, LysoPC C18:0 reduced the metastatic spread of murine melanoma B16.F10 cells in mice. Although membrane rigidification may have a key role in the attenuation of metastasis, evidence for this has yet to be shown. Therefore, the present study aimed to determine how LysoPC reduces the metastatic capacity of B16.F10 cells. Following cellular preincubation with LysoPC C18:0 at increasing concentrations and lengths of time, cell migration was most significantly attenuated with 450 μm LysoPC C18:0 at 72 h. Biosensor measurements suggest that, despite their abundance in B16.F10 cells, LysoPC-sensitive G protein-coupled receptors do not appear to contribute to this effect. Instead, the attenuated migration appears to result from changes in cell membrane properties and their effect on underlying signaling pathways, most likely the formation of focal adhesion complexes. Treatment with 450 μm LysoPC C18:0 activates protein kinase C (PKC)δ to phosphorylate syndecan-4, accompanied by deactivation of PKCα. Subsequently, focal adhesion complex formation was attenuated, as confirmed by the reduced activity of focal adhesion kinase (FAK). Interestingly, 450 μm LysoPC C18:1 did not affect FAK activity, explaining its lower propensity to affect migration and metastasis. Therefore, membrane rigidification by LysoPC C18:0 appears to prevent the formation of focal adhesion complexes, thus affecting integrin activity as a key for metastatic melanoma spread.

Indexed as

cancerG protein‐coupled receptorintegrinlysophospholipidmetastasis

Identifiers

PMID28255537
PMCPMC5324772
OpenAlexW2548755103

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.