ArticleCell communication and signaling : CCS2024
Arachidonic acid impairs natural killer cell functions by disrupting signaling pathways driven by activating receptors and reactive oxygen species.
Article in Cell communication and signaling : CCS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Differential modulation of gestational immunity by fatty acids: tissue-specific immune remodeling and clinical implications.Clinical science (London, England : 1979) · 2026Article
- Characterizing tumor microenvironment heterogeneity in EBVFrontiers in immunology · 2026Article
- Loss of MFE-2 impairs microglial lipid homeostasis and drives neuroinflammation in Alzheimer's pathogenesis.Nature aging · 2025Article
- Metabolomics Analysis of the Mechanism of Yuquan Capsules in the Treatment of T2DM Rats Using UPLC/MS.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025Article
- Crosstalk between stromal, immune, and ovarian cancer cells in lipid-rich tumor microenvironment exhibits proliferative features.Frontiers in immunology · 2025Review
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Authors and funding
11 authors.
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Abstract
backgroundHigh levels of the polyunsaturated fatty acid arachidonic acid (AA) within the ovarian carcinoma (OC) microenvironment correlate with reduced relapse-free survival. Furthermore, OC progression is tied to compromised immunosurveillance, partially attributed to the impairment of natural killer (NK) cells. However, potential connections between AA and NK cell dysfunction in OC have not been studied.
methodsWe employed a combination of phosphoproteomics, transcriptional profiling and biological assays to investigate AA's impact on NK cell functions.
resultsAA (i) disrupts interleukin-2/15-mediated expression of pro-inflammatory genes by inhibiting STAT1-dependent signaling, (ii) hampers signaling by cytotoxicity receptors through disruption of their surface expression, (iii) diminishes phosphorylation of NKG2D-induced protein kinases, including ERK1/2, LYN, MSK1/2 and STAT1, and (iv) alters reactive oxygen species production by transcriptionally upregulating detoxification. These modifications lead to a cessation of NK cell proliferation and a reduction in cytotoxicity.
conclusionOur findings highlight significant AA-induced alterations in the signaling network that regulates NK cell activity. As low expression of several NK cell receptors correlates with shorter OC patient survival, these findings suggest a functional linkage between AA, NK cell dysfunction and OC progression.
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