Communication between human macrophages and epithelial cancer cell lines dictates lipid mediator biosynthesis

Werner, Markus; Czapka, Anna; Jordan, Paul M.; Gerstmeier, Jana; Koeberle, Andreas; Werz, Oliver

doi:10.1007/s00018-019-03413-w

Cited by 8 publications

(9 citation statements)

References 61 publications

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“…Thus, regulation of macrophage polarization using RvDs may be a potential therapeutic approach in the management of prostate cancer ( Shan et al, 2020 ) . The communication between human monocyte-derived M2-like macrophages (MDM) and cancer cells in co-incubations can strikingly modulate the biosynthetic capacities to produce bioactive LM including lipoxin A 4 , resolvin D2 and D5 were elevated after coculture with human A549 epithelial lung carcinoma cells ( Werner et al, 2020 ).…”

Section: Therapeutic Approachesmentioning

confidence: 99%

Carcinogenesis: Failure of resolution of inflammation?

Fishbein

Hammock

Serhan

et al. 2021

Pharmacology & Therapeutics

142

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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: Therapeutic Approachesmentioning

confidence: 99%

Carcinogenesis: Failure of resolution of inflammation?

Fishbein

Hammock

Serhan

et al. 2021

Pharmacology & Therapeutics

142

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“…We respectfully disagree with this assertion and point of view. Firstly, because as detailed above, there is extensive documentation from many groups (including some of the co-authors of O’Donnell et al 1, 2, 3, 4, 5, 6, 7, 8 ) which identify and quantitate SPM in an array of biological systems. Indeed, as discussed above, a PubMed search term of “resolvins” gives 1,420 reports (as of today) from groups around the world using commercially available resolvins and other SPMs confirming their potent stereoselective actions in a wide range of models and presence in human tissue samples 3, 9, 10, 11, 12, 13, 14, 15, 16 .…”

Section: Main Textmentioning

confidence: 99%

Evidence for the presence and diagnostic utility of SPM in human peripheral blood

Dalli

Gómez

Serhan

2022

Preprint

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SummaryWe thank O’Donnell et al, for their comments on our contribution and are grateful to be afforded this opportunity to formally respond to their critique24.We are surprised by the author’s assertion relating to the biological relevance of SPM because a simple literature search for related terms such as ‘resolvin’ in PubMed yields an abundance (>1,420 publications) of evidence supporting the potent biological activities and the diagnostic potential of some of these mediators. Several co-authors of the O’Donnell’s et al manuscript, have published on the resolvins and SPMs, including some publications within recent weeks. Importantly, O’Donnell et al, misreport as well as mis-apply criteria for peak identification reported in the Gomez et al, publication which lead to the flawed analysis they performed.In this response therefore, we provide a step-by-step clarification of the methodologies used in Gomez et al, and a side-by-side comparison of the underlying data to clarify any confusion. We also demonstrate that using the orthogonal criteria discussed by O’Donnell et al, we obtain essentially identical results thus providing additional validation of our techniques and support the conclusions.

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“…For example, LXA4 deficiency is associated with cystic fibrosis and severe asthma ( 34 , 35 ). Regarding cancers, overexpression of COX-2, 5-LOX and high levels of PG- and LT-derived metabolites that have important roles in tumor progression have been reported in many tumors ( 36 , 37 ). Contrarily, to date, few studies have investigated the potential relationship between SPM levels and cancer.…”

Section: Spms Mediate Resolution Of Inflammationmentioning

confidence: 99%

“…Of importance, cancer cells indirect interactions with TAM-like in vitro alter the lipid mediator profile produced by cancer cells toward the synthesis of pro-inflammatory PGs and LTs, with pro-tumorigenic properties ( 36 , 137 ). Among PGs, PGE2 largely contributes to tumor progression and promotes an immunosuppressive TME, particularly in macrophages ( 37 , 138 ).…”

Section: Macrophages Are Guardians Of Tissue Homeostasis and Key Regulators Of Pro-tumor Inflammationmentioning

confidence: 99%

Specialized Pro-Resolving Mediators Mitigate Cancer-Related Inflammation: Role of Tumor-Associated Macrophages and Therapeutic Opportunities

et al. 2021

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Inflammation is a fundamental physiological response orchestrated by innate immune cells to restore tissue homeostasis. Specialized pro-resolving mediators (SPMs) are involved in active resolution of inflammation but when inflammation is incomplete, chronic inflammation creates a favorable environment that fuels carcinogenesis and cancer progression. Conventional cancer therapy also strengthens cancer-related inflammation by inducing massive tumor cell death that activate surrounding immune-infiltrating cells such as tumor-associated macrophages (TAMs). Macrophages are key actors of both inflammation and its active resolution due to their plastic phenotype. In line with this high plasticity, macrophages can be hijacked by cancer cells to support tumor progression and immune escape, or therapy resistance. Impaired resolution of cancer-associated inflammation supported by TAMs may thus reinforces tumor progression. From this perspective, recent evidence suggests that stimulating macrophage’s pro-resolving functions using SPMs can promote inflammation resolution in cancer and improve anticancer treatments. Thus, TAMs’ re-education toward an antitumor phenotype by using SPMs opens a new line of attack in cancer treatment. Here, we review SPMs’ anticancer capacities with special attention regarding their effects on TAMs. We further discuss how this new therapeutic approach could be envisioned in cancer therapy.

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Communication between human macrophages and epithelial cancer cell lines dictates lipid mediator biosynthesis

Cited by 8 publications

References 61 publications

Carcinogenesis: Failure of resolution of inflammation?

Carcinogenesis: Failure of resolution of inflammation?

Evidence for the presence and diagnostic utility of SPM in human peripheral blood

Specialized Pro-Resolving Mediators Mitigate Cancer-Related Inflammation: Role of Tumor-Associated Macrophages and Therapeutic Opportunities

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