Effect of prostaglandins and hormones on cyclic AMP formation in rat hepatomas and liver tissue

Brønstad, Gunnar; Christoffersen, Thoralf; Johansen, Ellen J.; I, Oye

doi:10.1038/bjc.1978.281

Cited by 10 publications

(4 citation statements)

References 23 publications

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“…Surprisingly we found an interspecies difference concerning the number of binding sites between rat and human liver. Since rat hepatomas have an increased PGE1-sensitive adenylate cyclase activity and produce increased amounts of cAMP (Allen et al, 1971;Bronstad et al, 1978, Bronstad & Christofferson, 1981, Chayoth et al, 1973 we addressed the question of whether the binding capacity for PGE1 would be affected in human hepatocellular cancers.…”

mentioning

confidence: 99%

Human hepatocellular cancers show decreased prostaglandin E1 binding capacity

Virgolini¹,

Sinzinger²,

Müller³

et al. 1989

Br J Cancer

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confidence: 99%

Human hepatocellular cancers show decreased prostaglandin E1 binding capacity

Virgolini¹,

Sinzinger²,

Müller³

et al. 1989

Br J Cancer

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“…It has long been suspected that PGs and cAMP are involved in cell growth and cancer development [99] but this seems to be dependent on which specific PG is involved. PGF1alpha (PGF1a) and PGF2alpha (PGF2a) do not increase cAMP but 2-acetylaminofluorene (AAF)-induced cancer is associated with increased prostaglandin E1 (PGE1) [100].…”

Section: Eicosanoidsmentioning

confidence: 99%

Eicosanoids in carcinogenesis

Brücher

Jamall

2019

4open

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Inflammation is the body's reaction to pathogenic (biological or chemical) stimuli and covers a burgeoning list of compounds and pathways that act in concert to maintain the health of the organism. Eicosanoids and related fatty acid derivatives can be formed from arachidonic acid and other polyenoic fatty acids via the cyclooxygenase and lipoxygenase pathways generating a variety of pro- and anti-inflammatory mediators, such as prostaglandins, leukotrienes, lipoxins, resolvins and others. The cytochrome P450 pathway leads to the formation of hydroxy fatty acids, such as 20-hydroxyeicosatetraenoic acid, and epoxy eicosanoids. Free radical reactions induced by reactive oxygen and/or nitrogen free radical species lead to oxygenated lipids such as isoprostanes or isolevuglandins which also exhibit pro-inflammatory activities. Eicosanoids and their metabolites play fundamental endocrine, autocrine and paracrine roles in both physiological and pathological signaling in various diseases. These molecules induce various unsaturated fatty acid dependent signaling pathways that influence crosstalk, alter cell–cell interactions, and result in a wide spectrum of cellular dysfunctions including those of the tissue microenvironment. Although the complete role of eicosanoids, including that of the recently elucidated anti-inflammatory specialized pro-resolving lipid mediators (SPMs), e.g. lipoxins, resolvins, protectins and maresins, is not completely understood, the result of unremitting chronic inflammation is fostering early stages of carcinogenesis. Chronic inflammation facilitates the transition from a normal cell to a cancerous one. The disruption of homeostasis across a wide, but identifiable, swath of diverse molecular pathways creates a micromilieu which constitutes an early and necessary step in the 6-step sequence of carcinogenesis for the vast majority of cancers, termed “sporadic cancers”.

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“…Prostaglandins are associated with the activation of the adenylate cyclase-cAMP-system through specifically membrane bound receptors that have been demonstrated in several tissue fractions or at cell surface membranes (e.g., Hall & Strange, 1984, Riicker & Schr6r, 1983Virgolini, 1987). Increased response to prostaglandins by measuring the cAMP content in neoplastic tissue has been observed in various studies (e.g., Bronsted et al, 1978;Chayoth et al, 1973), thus prostaglandins are proposed to take part in cellular growth (Feher & Gridali, 1974;Hial et al, 1976). For thyroid cancer the effects of prostaglandins and of their synthesis inhibitors aspirin or indomethacine have been rarely reported in the literature (Sand et al, 1976), although an alteration in adenylate cyclase activity has been indicated in thyroid cancers (De Rubertis et al, 1972;Orgiazzi et al, 1977).…”

mentioning

confidence: 92%