ArticleBiochemical pharmacology2007
Activation of thromboxane receptor alpha induces expression of cyclooxygenase-2 through multiple signaling pathways in A549 human lung adenocarcinoma cells.
Article in Biochemical pharmacology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
13 citing papers in PubMed, 28 citations in OpenAlex.
- Role of nitric oxide, prostaglandins, thromboxanes and endothelins in lung cancer: An overview.World journal of clinical cases · 2025Review
- TIPRL Regulates Stemness and Survival in Lung Cancer Stem Cells through CaMKK2-CaMK4-CREB Feedback Loop Activation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Oncopreventive and oncotherapeutic potential of licorice triterpenoid compound glycyrrhizin and its derivatives: Molecular insights.Pharmacological research · 2022Review
- Thromboxane A2 exerts promoting effects on cell proliferation through mediating cyclooxygenase-2 signal in lung adenocarcinoma cells.Journal of cancer research and clinical oncology · 2014Article
- 18β-Glycyrrhetinic acid suppresses cell proliferation through inhibiting thromboxane synthase in non-small cell lung cancer.PloS one · 2014Article
- Article
- Cyclooxygenases and lipoxygenases in cancer.Cancer metastasis reviews · 2011Review
- Basic aspects of tumor cell fatty acid-regulated signaling and transcription factors.Cancer metastasis reviews · 2011Review
- The thromboxane synthase and receptor signaling pathway in cancer: an emerging paradigm in cancer progression and metastasis.Cancer metastasis reviews · 2011Review
- 4-Methylnitrosamino-1-3-pyridyl-1-butanone (NNK) promotes lung cancer cell survival by stimulating thromboxane A2 and its receptor.Oncogene · 2011Article
- Redox Factor-1 Inhibits Cyclooxygenase-2 Expression via Inhibiting of p38 MAPK in the A549 Cells.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2010Article
- CREB in the pathophysiology of cancer: implications for targeting transcription factors for cancer therapy.Clinical cancer research : an official journal of the American Association for Cancer Research · 2009Article
- In Vivo Cellular Imaging for Translational Medical Research.Current medical imaging reviews · 2009Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 3 countries.
Funding
Abstract
Human lung adenocarcinoma A549 cells stably transfected with TPalpha (A549-TPalpha) were used to study agonist I-BOP-induced expression of cyclooxygenase-2 (COX-2) and the related mechanisms of induced expression. I-BOP, a TP agonist, induced a time- and dose-dependent expression of COX-2 in A549-TPalpha cells. The signaling pathways of I-BOP-induced COX-2 expression were elucidated by using various inhibitors of the signaling molecules. The effects of these inhibitors were assessed at protein level, enzyme activity and promoter activity of COX-2. Within MAPK family, both ERK and p38 MAPK but not JNK/SAPK pathways were involved in the induction. Other pathways such as JAK/Stat3 pathway and beta-catenin/TCF/LEF pathway also participated in the induction. The activation of key signaling molecules, ERK, p38 MAPK, CREB and NF-kappaB, involved in the COX-2 transcription was further studied at the phosphorylation step. Activation of ERK and p38 MAPK appeared to be mediated primarily by transactivation of EGFR, whereas activation of CREB and NF-kappaB was mediated by PKA, PKC and ERK. The role of CREB and NF-kappaB in I-BOP-induced COX-2 expression was further explored at the promoter level. Studies on promoter fragments and mutation of responsive motifs indicated that CRE and NF-kappaB sites are critical for the COX-2 induction. Distal NF-kappaB site is essential for the basal induction of the COX-2 transcription, whereas CRE and proximal NF-kappaB sites are important for the induced transcription. These results indicate that I-BOP-induced COX-2 expression through multiple signaling pathways.
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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.