ArticleInflammation2015
Lipoxin A4 suppresses lipopolysaccharide-induced hela cell proliferation and migration via NF-κB pathway.
Article in Inflammation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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The trial behind it
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Who cites it
11 citing papers in PubMed, 23 citations in OpenAlex.
- Plasma lipoxin AMolecular carcinogenesis · 2017Trial
- Distinct colitis-associated macrophages drive NOD2-dependent bacterial sensing and gut homeostasis.The Journal of clinical investigation · 2025Article
- Pro- and anti-inflammatory bioactive lipids imbalance contributes to the pathobiology of autoimmune diseases.European journal of clinical nutrition · 2023Review
- Impact of variability in cell cycle periodicity on cell population dynamics.PLoS computational biology · 2023Article
- Inflammation and tumor progression: signaling pathways and targeted intervention.Signal transduction and targeted therapy · 2021Article
- Metabolism pathways of arachidonic acids: mechanisms and potential therapeutic targets.Signal transduction and targeted therapy · 2021Review
- PUFAs, BDNF and lipoxin A4 inhibit chemical-induced cytotoxicity of RIN5F cells in vitro and streptozotocin-induced type 2 diabetes mellitus in vivo.Lipids in health and disease · 2019Article
- Docosahexaenoic Acid Suppresses Silica-Induced Inflammasome Activation and IL-1 Cytokine Release by Interfering With Priming Signal.Frontiers in immunology · 2019Article
- Resolution of Cancer-Promoting Inflammation: A New Approach for Anticancer Therapy.Frontiers in immunology · 2017Review
- Anti-inflammatory properties of lipoxin A4 protect against diabetes mellitus complicated by focal cerebral ischemia/reperfusion injury.Neural regeneration research · 2016Article
- Lipoxin A4 Preconditioning Attenuates Intestinal Ischemia Reperfusion Injury through Keap1/Nrf2 Pathway in a Lipoxin A4 Receptor Independent Manner.Oxidative medicine and cellular longevity · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Uterine cervical carcinoma (UCC) is one of the most common malignant tumors in females, and UCC has a close relationship with chronic cervicitis. As the endogenous "braking signal," lipoxins can regulate anti-inflammation and the resolution of inflammation. We investigated the effect of lipoxin A4 (LXA4) on the proliferation, apoptosis, and migration in lipopolysaccharide (LPS)-stimulated Hela cells. We demonstrated that LXA4 could significantly suppress p53, cyclin D1 expression, and migration of LPS-stimulated Hela cells via nuclear factor-κB (NF-κB) pathway, and these effects could be blocked by Boc-2, the specific inhibitor of FPR2/ALX (the receptor of LXA4). We presented evidence for a novel role of LXA4 on the proliferation and migration in LPS-stimulated Hela cells, and FPR2/ALX was involved in the procedures. These results showed that LXA4 could be a possible candidate for UCC therapy, and blocking the activation of NF-κB would be an effective drug target.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.