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• W2074587514 abstract "Arachidonic acid and certain highly unsaturated fatty acids can serve as signals controlling the proliferation and death of mammalian cells (Table 1). Arachidonic acid is released from membrane phospholipids after stimulation with cytokines, growth factors and various environmental stimuli. Once released, arachidonic acid may be rapidly converted into eicosanoids, leukotrienes and other metabolites. Although these metabolites influence several cellular processes, arachidonic acid itself is involved in the regulation of diverse cellular functions. Thus many studies have implicated arachidonic acid as a mediator of growth factor-dependent activation of signalling pathways involved in the regulation of gene expression. The scope of the following group of papers is to present evidence that arachidonic acid-associated signals impinge on the processes of cell growth and survival. Particular attention will be placed on neoplasms, in the light of advances in knowledge of regulatory genes, physiological and pathological processes and potential therapeutic interventions. Novel aspects of arachidonic acid biology and highly unsaturated fatty acid signalling will be discussed. The inspiration for some of these studies arose from Floyd Chilton’s group, who first implicated arachidonic acid metabolism in the process of apoptosis, describing the link between arachidonate-phospholipid remodelling and apoptosis. 1 In this edition, Chilton’s group will describe a continuation of this work in their recent studies on the arachidonyl transacylase in squamous cell carcinoma, which suggests that increasing intracellular arachidonic acid inhibited tumour growth. They will also describe recent studies on a signalling pathway associated with the Peroxisome Proliferator Activated Receptor gamma (PPARg), a transcription factor that drives expression of specific genes when activated by naturally occurring metabolites of arachidonic acid. The direct action of arachidonic acid and highly unsaturated fatty acids on gene expression has been investigated in the signal transduction laboratory of Maria Teresa Rizzo (Fig. 1). Rizzo will describe the activation of stress kinase pathways and the control of cell proliferation and activation of stress kinase pathways by arachidonic acid. A link with early advances in arachidonic acid signalling was provided by David Horrobin, who was a student of the nutritional biochemist Hugh Sinclair, who formulated many of the initial hypotheses linking arachidonic acid metabolism to cancer and cardiovascular disease. 2 David Horrobin has extended these observations and hypotheses into many areas of cell transformation and signalling. 3 Horrobin discussed the role of highly unsaturated fatty acids as intracellular mediators of various cytokines, including work on studies on the fatty acid composition of tumours and important studies indicating involvement of highly unsaturated fatty acids in long-term potentiation. In terms of therapeutic advances in oncology, interest has recently centred on the modulation of cyclooxygenase (COX) activity, using specific inhibitors of the inducible COX-2 enzyme whose expression is upregulated in various tumour types. The potential for COX inhibitors to inhibit angiogenesis and tumour growth in a variety of epithelial and endothelial tumours is described by Alane Koki and colleagues. Encouraging trials using these more specific inhibitors suggest that COX-2 inhibitors may be used to prevent or treat certain neoplasms. The question of how the COX inhibitors act, however, remains highly contentious. Do COX-2 inhibitors act directly, by simply blocking the COX-2 enzyme, or do they stimulate tumour cell death by other routes such as cyclic GMP, Bcl-XL, PPAR, NF-KB and I-KB? The metabolism of highly unsaturated fatty acids is also discussed in" @default.
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• W2074587514 date "2002-01-01" @default.
• W2074587514 modified "2023-09-26" @default.
• W2074587514 title "Antitumour actions of highly unsaturated fatty acids: cell signalling and apoptosis" @default.
• W2074587514 cites W1529151652 @default.
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• W2074587514 doi "https://doi.org/10.1054/plef.2001.0333" @default.
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