ArticleScientific reports2017
Elevated COX-2 Expression Promotes Angiogenesis Through EGFR/p38-MAPK/Sp1-Dependent Signalling in Pancreatic Cancer.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.
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Who cites it
48 citing papers in PubMed, 1 synthesis or guideline pooled it, 100 citations in OpenAlex.
- Prognostic Value of COX-2, NF-κB, and Sp1 Tissue Expressions in Pancreatic Ductal Adenocarcinoma: A Systematic Review and Meta-analysis.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2021Pooled it
- The Role ofMedicina (Kaunas, Lithuania) · 2020Trial
- Quinazolinone-diarylpyrazole hybrids as dual EGFR/COX-2 inhibitors: antiproliferative, mechanistic, andRSC advances · 2026Article
- An In Silico Study of Resveratrol Derivatives as Dual Inhibitors of Cyclooxygenase-2 (COX-2) and 5-Lipoxygenase (5-LOX) in Cancer Therapy.Biotechnology and applied biochemistry · 2026Article
- Modulation of tumor-derived exosomes and reprogramming of cancer-associated fibroblasts for colorectal cancer therapy.Molecular cancer · 2026Article
- COL1A1-induced LOXL2 promotes ovarian cancer metastasis via a feedback loop upon inhibiting EGFR lysosomal degradation.Experimental & molecular medicine · 2026Article
- Sodium new houttuyfonate affects tumor angiogenesis by suppressing FGF1 expression and the p38/MAPK signaling pathway in pancreatic cancer.Scientific reports · 2025Article
- Decoding intratumoral cyclooxygenase-2 signaling through multi-omics: insights from esophageal cancer and beyond.Clinical and experimental medicine · 2025Article
- Gemcitabine and Flurbiprofen Enhance Cytotoxic Effects on Cancer Cell Lines Mediated by Mesenchymal Stem Cells.International journal of molecular sciences · 2025Article
- SHP1 and its downstream p38/SP1/PI3K/YAP/Notch-1 signaling in trophoblast cells suppressed the progression of Preeclampsia via inhibiting proliferation of SMCs.Scientific reports · 2025Article
- GLI2 Facilitates Tumor Immune Evasion and Immunotherapeutic Resistance by Coordinating WNT and Prostaglandin Signaling.Cancer research · 2025Article
- Zapotin mitigates breast cancer progression by targeting PKCε mediated glycolytic pathway regulation.BMC cancer · 2025Article
- Arachidonic acid metabolism as a novel pathogenic factor in gastrointestinal cancers.Molecular and cellular biochemistry · 2025Review
- Reduced expression of UPF1 promotes tumor progression through stabilizing COX-2 mRNA in nasopharyngeal carcinoma.Frontiers in immunology · 2025Article
- Repurposing of Indomethacin and Naproxen as anticancer agents: progress from 2017 to present.RSC advances · 2024Review
- SP1 undergoes phase separation and activates RGS20 expression through super-enhancers to promote lung adenocarcinoma progression.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- The cyclooxygenase-2 upregulation mediates production of PGE2 autacoid to positively regulate interleukin-6 secretion in chronic rhinosinusitis with nasal polyps and polyp-derived fibroblasts.Scientific reports · 2024Article
- Recent Advancements in Refashioning of NSAIDs and their Derivatives as Anticancer Candidates.Current pharmaceutical design · 2024Review
- Role of Leptin and Adiponectin in Carcinogenesis.Cancers · 2023Review
- Article
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9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cyclooxygenase-2 (COX-2) was stated to be overexpression in various human malignancies associating with angiogenesis, metastasis and chemoresistence. Pancreatic ductal adenocarcinoma (PDAC) is a lethal disease displaying many of these characteristics. A common abnormality of PDAC is overexpression of specificity protein-1 (Sp1), which was said to correlate with malignant phenotypes of human cancers. Using RNA-seq data from The Cancer Genome Atlas (TCGA), we found that Sp1 expression was positively correlated with that of COX-2 in PDAC, and that the inhibition or overexpression of Sp1 in PDAC cells leads to decreased or elevated COX-2 expression. Luciferase reporter gene and chromatin immunoprecipitation (ChIP) assays revealed that elevated transcription of COX-2 requires Sp1 binding to sequence positions around -245/-240 of COX-2 promoter. Activated epidermal growth factor receptor (EGFR) and downstream p38 mitogen-activated protein kinase (p38-MAPK) were also profoundly altered in PDAC. The inhibition of EGFR/p38-MAPK signaling resulted in reduced Sp1 activation, decreased COX-2 and vascular endothelial growth factor (VEGF) expression. Thus, Sp1 could transcriptionally activate COX-2 expression in a process relies on activated EGFR/p38-MAPK signaling. Finally, we found that the inhibition of COX-2 leads to decreased angiogenesis in a process dependent on VEGF, which link COX-2 to angiogenesis in PDAC.
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