Lysophosphatidylcholine attenuates melanoma cell adhesion and migration dependent on the degree of fatty acid saturation

Ross, Thomas; Heuter, Sebastian; Schlesinger, Martin; Jakubzig, Bastian; Raynor, Anna; Massing, Ulrich; Bendas, Gerd

doi:10.5414/cpxces14ea05

Cited by 2 publications

(2 citation statements)

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“…Because there appears to be no preference for specific lipid species and a high tolerance for their membrane incorporation by transacylation [9], FAs biophysically affect the membrane properties in relation to their degree of saturation. Consequently, saturated FAs such as stearic acid (C18:0) mediate a rigidification of the tumor cell membrane, which we could demonstrate by FRAP experiments (B16.F10 cells) or by fluorescence anisotropy using 1-(4-trimethylammoniumphenyl)-6phenyl-1,3,5-hexatriene p-toluenesulfonate (MV3 human melanoma cells) in previous studies [9,43].…”

Section: Discussionmentioning

confidence: 68%

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

et al. 2016

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Lysophophatidylcholine (Lyso PC ) is an abundant constituent in human plasma. Patients with malignant cancer diseases have attenuated Lyso PC plasma levels, and thus Lyso PC has been examined as a metabolic biomarker for cancer prediction. Preclinical studies have shown that solid tumor cells drastically degrade Lyso PC s by incorporating their free fatty acids into cell membrane phospholipids. In this way, Lyso PC 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 Lyso PC reduces the metastatic capacity of B16.F10 cells. Following cellular preincubation with Lyso PC C18:0 at increasing concentrations and lengths of time, cell migration was most significantly attenuated with 450 μ m Lyso PC C18:0 at 72 h. Biosensor measurements suggest that, despite their abundance in B16.F10 cells, Lyso PC ‐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 μ m Lyso PC C18:0 activates protein kinase C ( PKC )δ to phosphorylate syndecan‐4, accompanied by deactivation of PKC α. Subsequently, focal adhesion complex formation was attenuated, as confirmed by the reduced activity of focal adhesion kinase ( FAK ). Interestingly, 450 μ m Lyso PC C18:1 did not affect FAK activity, explaining its lower propensity to affect migration and metastasis. Therefore, membrane rigidification by Lyso PC C18:0 appears to prevent the formation of focal adhesion complexes, thus affecting integrin activity as a key for metastatic melanoma spread.

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Section: Discussionmentioning

confidence: 68%

“…Cell migration assays were performed as described previously [43]. In total, 5000 B16.F10 cells were seeded on fibronectin coated (10 lgÁmL À1 ; Sigma-Aldrich Chemie GmbH) or uncoated 24-well plates (STARLAB GmbH, Hamburg, Germany).…”

Section: Cell Migrationmentioning

confidence: 99%

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

et al. 2016

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An Updated Review of Pro- and Anti-Inflammatory Properties of Plasma Lysophosphatidylcholines in the Vascular System

Knuplez

Marsche

2020

IJMS

100

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Lysophosphatidylcholines are a group of bioactive lipids heavily investigated in the context of inflammation and atherosclerosis development. While present in plasma during physiological conditions, their concentration can drastically increase in certain inflammatory states. Lysophosphatidylcholines are widely regarded as potent pro-inflammatory and deleterious mediators, but an increasing number of more recent studies show multiple beneficial properties under various pathological conditions. Many of the discrepancies in the published studies are due to the investigation of different species or mixtures of lysophatidylcholines and the use of supra-physiological concentrations in the absence of serum or other carrier proteins. Furthermore, interpretation of the results is complicated by the rapid metabolism of lysophosphatidylcholine (LPC) in cells and tissues to pro-inflammatory lysophosphatidic acid. Interestingly, most of the recent studies, in contrast to older studies, found lower LPC plasma levels associated with unfavorable disease outcomes. Being the most abundant lysophospholipid in plasma, it is of utmost importance to understand its physiological functions and shed light on the discordant literature connected to its research. LPCs should be recognized as important homeostatic mediators involved in all stages of vascular inflammation. In this review, we want to point out potential pro- and anti-inflammatory activities of lysophospholipids in the vascular system and highlight recent discoveries about the effect of lysophosphatidylcholines on immune cells at the endothelial vascular interface. We will also look at their potential clinical application as biomarkers.

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Lysophosphatidylcholine attenuates melanoma cell adhesion and migration dependent on the degree of fatty acid saturation

Cited by 2 publications

References 6 publications

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

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

An Updated Review of Pro- and Anti-Inflammatory Properties of Plasma Lysophosphatidylcholines in the Vascular System

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