Targeting lipid mediators in cancer biology

Sulciner, Megan L.; Gartung, Allison; Gilligan, Molly M.; Serhan, Charles N.; Panigrahy, Dipak

doi:10.1007/s10555-018-9754-9

Cited by 47 publications

(34 citation statements)

References 171 publications

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“…While carcinogens induce inflammation, a hallmark of cancer and a key characteristic of their pro-tumorigenic activity ( Hanahan & Weinberg, 2011 ; Mantovani et al, 2008 ; Smith et al, 2016 ), they also disrupt the resolution of inflammation. Thus, the loss of inflammation resolution is an emerging mechanism of cancer pathogenesis ( Gilligan et al, 2019 ; Liu et al, 2019 ; Panigrahy et al, 2019 ; Serhan & Levy, 2018 ; Sulciner, Gartung, et al, 2018 ; Sulciner, Serhan, et al, 2018 ; Ye et al, 2018 ). Carcinogens continue to play a large role in the disease and social burdens of cancer globally.…”

Section: Discussionmentioning

confidence: 99%

“…Chronic inflammation and infection contributes to about 25% of all human cancers, including various tumor types such as hepatocellular, bladder and prostate cancer ( De Marzo et al, 2007 ; Greene et al, 2011 ; Sulciner, Gartung, Gilligan, Serhan, & Panigrahy, 2018 ). For example, inflammation initiates cancer growth within 5 to 8 months in a genetically engineered model of pancreatic cancer ( Guerra et al, 2007 ).…”

Section: Inflammation and Cancermentioning

confidence: 99%

“…The trigger of dormancy escape, as numerous animal studies have shown, is typically of non-genetic nature and can include: wounding at a site near or distant from the site of the occult tumor, surgery, chemotherapy, radiation, biopsy, sustained inflammation, stimulated angiogenesis or the presence of non-mutagenic factors that perturb the metabolism of cells ( Panigrahy et al, 2012 ; Panigrahy et al, 2019 ). Cell death can paradoxically trigger dormancy escape by the stimulation of pro-inflammatory and pro-angiogenic cytokines which suggests that cell death generated by carcinogens can stimulate tumor growth ( Fishbein et al, 2020 ; Gartung et al, 2019 ; Sulciner, Gartung, et al, 2018 ). In experimental models, tumor dormancy escape can occur by 90 days post-tumor cell injection of dormant tumor cells by the stimulation of angiogenesis ( Panigrahy et al, 2012 ).…”

Section: Mechanisms Of Pro-tumorigenic Activity By Carcinogensmentioning

confidence: 99%

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Carcinogenesis: Failure of resolution of inflammation?

Fishbein

Hammock

Serhan

et al. 2021

Pharmacology & Therapeutics

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111

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Inflammation in the tumor microenvironment is a hallmark of cancer and is recognized as a key characteristic of carcinogens. However, the failure of resolution of inflammation in cancer is only recently being understood. Products of arachidonic acid and related fatty acid metabolism called eicosanoids, including prostaglandins, leukotrienes, lipoxins, and epoxyeicosanoids, critically regulate inflammation, as well as its resolution. The resolution of inflammation is now appreciated to be an active biochemical process regulated by endogenous specialized pro-resolving lipid autacoid mediators which combat infections and stimulate tissue repair/regeneration. Environmental and chemical human carcinogens, including aflatoxins, asbestos, nitrosamines, alcohol, and tobacco, induce tumor-promoting inflammation and can disrupt the resolution of inflammation contributing to a devastating global cancer burden. While mechanisms of carcinogenesis have focused on genotoxic activity to induce mutations, nongenotoxic mechanisms such as inflammation and oxidative stress promote genotoxicity, proliferation, and mutations. Moreover, carcinogens initiate oxidative stress to synergize with inflammation and DNA damage to fuel a vicious feedback loop of cell death, tissue damage, and carcinogenesis. In contrast, stimulation of resolution of inflammation may prevent carcinogenesis by clearance of cellular debris via macrophage phagocytosis and inhibition of an eicosanoid/cytokine storm of pro-inflammatory mediators. Controlling the host inflammatory response and its resolution in carcinogen-induced cancers will be critical to reducing carcinogen-induced morbidity and mortality. Here we review the recent evidence that stimulation of resolution of inflammation, including pro-resolution lipid mediators and soluble epoxide hydrolase inhibitors, may be a new chemopreventive approach to prevent carcinogen-induced cancer that should be evaluated in humans.

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Section: Discussionmentioning

confidence: 99%

Section: Inflammation and Cancermentioning

confidence: 99%

Section: Mechanisms Of Pro-tumorigenic Activity By Carcinogensmentioning

confidence: 99%

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Carcinogenesis: Failure of resolution of inflammation?

Fishbein

Hammock

Serhan

et al. 2021

Pharmacology & Therapeutics

Self Cite

111

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“…Many of the lipid-derived mediators are short-lived second messengers, and regulate cellular functions as migration, proliferation, apoptosis, redox balance, and cytoskeletal organization. Alteration or aberration in the generation of lipids mediators has been shown to regulate the physiology and pathophysiology of several disorders including, but not limited to, cancer, brain injury, cardiovascular diseases, kidney diseases, and pulmonary complications [1][2][3][4][5][6]. This review will specifically highlight the involvement of lipid mediators in pulmonary fibrosis (PF) and provide some mechanistic insights into the regulation of idiopathic pulmonary fibrosis (IPF) pathology by various lipid metabolites in animal models that mimic IPF.…”

Section: Introductionmentioning

confidence: 99%

Lipid Mediators Regulate Pulmonary Fibrosis: Potential Mechanisms and Signaling Pathways

Suryadevara

Ramchandran

Kamp

et al. 2020

IJMS

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Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease of unknown etiology characterized by distorted distal lung architecture, inflammation, and fibrosis. The molecular mechanisms involved in the pathophysiology of IPF are incompletely defined. Several lung cell types including alveolar epithelial cells, fibroblasts, monocyte-derived macrophages, and endothelial cells have been implicated in the development and progression of fibrosis. Regardless of the cell types involved, changes in gene expression, disrupted glycolysis, and mitochondrial oxidation, dysregulated protein folding, and altered phospholipid and sphingolipid metabolism result in activation of myofibroblast, deposition of extracellular matrix proteins, remodeling of lung architecture and fibrosis. Lipid mediators derived from phospholipids, sphingolipids, and polyunsaturated fatty acids play an important role in the pathogenesis of pulmonary fibrosis and have been described to exhibit pro- and anti-fibrotic effects in IPF and in preclinical animal models of lung fibrosis. This review describes the current understanding of the role and signaling pathways of prostanoids, lysophospholipids, and sphingolipids and their metabolizing enzymes in the development of lung fibrosis. Further, several of the lipid mediators and enzymes involved in their metabolism are therapeutic targets for drug development to treat IPF.

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“…Bioactive lipids comprise a variety of molecules, whose biosynthesis and activity are responsible for several cell functions, including cell membrane integrity, energy storage, and lipid signaling, by exchanges within and outside the cell [1,2]. The biosynthesis of many lipids depends on the presence of their precursors, and changes in lipid metabolism are involved both in physiological processes and in pathological conditions, such as inflammation, immune system diseases, and cancer [1][2][3][4][5]. Moreover, lipid moieties are necessary for the generation of lipid messengers, such as arachidonic acid (AA)-derived eicosanoids, endocannabinoids (ECs), and long-chain fatty acid derivatives such as N-acylethanolamides (NAEs), which modulate important cellular processes, such as proliferation, apoptosis, and inflammation.…”

Section: Bioactive Lipidsmentioning

confidence: 99%

Quantitative Lipidomic Analysis of Osteosarcoma Cell-Derived Products by UHPLC-MS/MS

et al. 2020

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Changes in lipid metabolism are involved in several pathological conditions, such as cancer. Among lipids, eicosanoids are potent inflammatory mediators, synthesized from polyunsaturated fatty acids (PUFAs), which coexist with other lipid-derived ones, including endocannabinoids (ECs) and N-acylethanolamides (NAEs). In this work, a bioanalytical assay for 12 PUFAs/eicosanoids and 20 ECs/NAEs in cell culture medium and human biofluids was validated over a linear range of 0.1–2.5 ng/mL. A fast pretreatment method consisting of protein precipitation with acetonitrile followed by a double step liquid–liquid extraction was developed. The final extracts were injected onto a Kinetex ultra-high-performance liquid chromatography (UHPLC) XB-C18 column with a gradient elution of 0.1% formic acid in water and methanol/acetonitrile (5:1; v/v) mobile phase. Chromatographic separation was followed by detection with a triple-quadrupole mass spectrometer operating both in positive and negative ion-mode. A full validation was carried out in a small amount of cell culture medium and then applied to osteosarcoma cell-derived products. To the best of our knowledge, this is the first lipid profiling of bone tumor cell lines (SaOS-2 and MG-63) and their secretome. Our method was also partially validated in other biological matrices, such as serum and urine, ensuring its broad applicability as a powerful tool for lipidomic translational research.

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Targeting lipid mediators in cancer biology

Cited by 47 publications

References 171 publications

Carcinogenesis: Failure of resolution of inflammation?

Carcinogenesis: Failure of resolution of inflammation?

Lipid Mediators Regulate Pulmonary Fibrosis: Potential Mechanisms and Signaling Pathways

Quantitative Lipidomic Analysis of Osteosarcoma Cell-Derived Products by UHPLC-MS/MS

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