Lipid composition of cultured B16 melanoma cell variants with different lung‐colonizing potential

Calorini, Lido; Fallani, Anna; Tombaccini, Donatella; Mugnai, Gabriele; Ruggieri, Salvatore

doi:10.1007/bf02533944

Cited by 16 publications

(13 citation statements)

References 41 publications

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“…2, 3). Reports that B16 melanomas produce almost entirely GM3 (∼95%), with the remainder consisting of GM2, GM1, and possibly GD1a [61] support the conclusion that SBD indeed prefers high concentrations of more complex ganglioside species (such as GT1b, GD1b, or GQ1b; see fig. 4) in which this cell line is deficient.…”

Section: Resultsmentioning

confidence: 78%

A Fluorescent Glycolipid-Binding Peptide Probe Traces Cholesterol Dependent Microdomain-Derived Trafficking Pathways

et al. 2008

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BackgroundThe uptake and intracellular trafficking of sphingolipids, which self-associate into plasma membrane microdomains, is associated with many pathological conditions, including viral and toxin infection, lipid storage disease, and neurodegenerative disease. However, the means available to label the trafficking pathways of sphingolipids in live cells are extremely limited. In order to address this problem, we have developed an exogenous, non-toxic probe consisting of a 25-amino acid sphingolipid binding domain, the SBD, derived from the amyloid peptide Aβ, and conjugated by a neutral linker with an organic fluorophore. The current work presents the characterization of the sphingolipid binding and live cell trafficking of this novel probe, the SBD peptide. SBD was the name given to a motif originally recognized by Fantini et al [1] in a number of glycolipid-associated proteins, and was proposed to interact with sphingolipids in membrane microdomains.Methodology/Principal FindingsIn accordance with Fantini's model, optimal SBD binding to membranes depends on the presence of sphingolipids and cholesterol. In synthetic membrane binding assays, SBD interacts preferentially with raft-like lipid mixtures containing sphingomyelin, cholesterol, and complex gangliosides in a pH-dependent manner, but is less glycolipid-specific than Cholera toxin B (CtxB). Using quantitative time-course colocalization in live cells, we show that the uptake and intracellular trafficking route of SBD is unlike that of either the non-raft marker Transferrin or the raft markers CtxB and Flotillin2-GFP. However, SBD traverses an endolysosomal route that partially intersects with raft-associated pathways, with a major portion being diverted at a late time point to rab11-positive recycling endosomes. Trafficking of SBD to acidified compartments is strongly disrupted by cholesterol perturbations, consistent with the regulation of sphingolipid trafficking by cholesterol.Conclusions/SignificanceThe current work presents the characterization and trafficking behavior of a novel sphingolipid-binding fluorescent probe, the SBD peptide. We show that SBD binding to membranes is dependent on the presence of cholesterol, sphingomyelin, and complex glycolipids. In addition, SBD targeting through the endolysosomal pathway in neurons is highly sensitive to cholesterol perturbations, making it a potentially useful tool for the analysis of sphingolipid trafficking in disease models that involve changes in cholesterol metabolism and storage.

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Section: Resultsmentioning

confidence: 78%

A Fluorescent Glycolipid-Binding Peptide Probe Traces Cholesterol Dependent Microdomain-Derived Trafficking Pathways

et al. 2008

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“…Because tumor cells rely mostly on glycolysis rather than on mitochondrial respiration (42), they are less effective than normal cells in generating ATP that is required for the internalization of exogenously added phosphatidylserine. It is also possible that integration of phosphatidylserine into plasma membrane of tumor cells from liposomes may be lessened by the specifics of their membrane lipid composition (43). We found that phosphatidylserine-containing ointment significantly inhibited tumor growth.…”

Section: Discussionmentioning

confidence: 99%

Recognition of Live Phosphatidylserine-Labeled Tumor Cells by Dendritic Cells: A Novel Approach to Immunotherapy of Skin Cancer

et al. 2009

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Dendritic cells (DC) loaded with tumor antigens from apoptotic/necrotic tumor cells are commonly used as vaccines for cancer therapy. However, the use of dead tumor cells may cause both tolerance and immunity, making the effect of vaccination unpredictable. To deliver live tumor “cargoes” into DC, we developed a new approach based on the “labeling” of tumors with a phospholipid “eat-me” signal, phosphatidylserine. Expression of phosphatidylserine on live tumor cells mediated their recognition and endocytosis by DC resulting in the presentation of tumor antigens to antigen-specific T cells. In mice, topical application of phosphatidylserine-containing ointment over melanoma induced tumor-specific CTL, local and systemic antitumor immunity, and inhibited tumor growth. Thus, labeling of tumors with phosphatidylserine is a promising strategy for cancer immunotherapy.

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“…After conversion to prostaglandins (PG), leukotrienes, or oxygen-derived free radicals, they mediate a variety of pathological processes (1). The PUFA content is drastically decreased in hepatoma cells in comparison with normal hepatocytes (2), in glioma cells in comparison with oligodendroglia cells (3,4) and in melanoma cells (5). This deficiency may cause alterations in signal transduction and an interruption of normal cellular events (3).…”

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confidence: 98%

Dose‐dependent inhibition of cell proliferation induced by lipid peroxidation products in rat hepatoma cells after enrichment with arachidonic acid

Muzio

Salvo

Trombetta

et al. 1999

Lipids

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Polyunsaturated fatty acids (PUFA) are important constituents of membrane phospholipids, whose levels are decreased in some tumor cells. This deficiency may cause alterations in signal transduction and an interruption of normal cellular events. The enrichment of tumor cells with PUFA may stimulate or inhibit tumor growth, probably depending on the type of PUFA and the cellular concentration of aldehydes derived from restored lipid peroxidation. We examined the effect of several doses of prooxidant on the growth of hepatoma cells with different aldehyde dehydrogenase activities, enriched with arachidonic acid. Two doses of prooxidant were sufficient to reduce growth of hepatoma cells with low aldehyde dehydrogenase activity, whereas three doses were necessary for those with high enzyme activity. In both cases, lipid peroxidation products blocked the cells in the S phase.

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Lipid composition of cultured B16 melanoma cell variants with different lung‐colonizing potential

Cited by 16 publications

References 41 publications

A Fluorescent Glycolipid-Binding Peptide Probe Traces Cholesterol Dependent Microdomain-Derived Trafficking Pathways

A Fluorescent Glycolipid-Binding Peptide Probe Traces Cholesterol Dependent Microdomain-Derived Trafficking Pathways

Recognition of Live Phosphatidylserine-Labeled Tumor Cells by Dendritic Cells: A Novel Approach to Immunotherapy of Skin Cancer

Dose‐dependent inhibition of cell proliferation induced by lipid peroxidation products in rat hepatoma cells after enrichment with arachidonic acid

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