ArticleCarcinogenesis2009
Tolfenamic acid inhibits esophageal cancer through repression of specificity proteins and c-Met.
Article in Carcinogenesis, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
36 citing papers in PubMed, 79 citations in OpenAlex.
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- Review
- NOS2 and COX-2 Co-Expression Promotes Cancer Progression: A Potential Target for Developing Agents to Prevent or Treat Highly Aggressive Breast Cancer.International journal of molecular sciences · 2024Review
- SP4 Facilitates Esophageal Squamous Cell Carcinoma Progression by Activating PHF14 Transcription and Wnt/Β-Catenin Signaling.Molecular cancer research : MCR · 2024Article
- Sp1 Targeted PARP1 Inhibition Protects Cardiomyocytes From Myocardial Ischemia-Reperfusion Injury via Downregulation of Autophagy.Frontiers in cell and developmental biology · 2021Article
- PI3K-targeting strategy using alpelisib to enhance the antitumor effect of paclitaxel in human gastric cancer.Scientific reports · 2020Article
- Next generation sequencing and functional pathway analysis to understand the mechanism of action of copper-tolfenamic acid against pancreatic cancer cells.Process biochemistry (Barking, London, England) · 2020Article
- Synergistic effect of tolfenamic acid and glycyrrhizic acid on TPA-induced skin inflammation in mice.MedChemComm · 2019Article
- Effect of Selected Nonsteroidal Anti-inflammatory Drugs on the Viability of Canine Osteosarcoma Cells of the D-17 Line:Journal of veterinary research · 2019Article
- SP and KLF Transcription Factors in Digestive Physiology and Diseases.Gastroenterology · 2017Review
- Targeting specificity protein 1 transcription factor and survivin using tolfenamic acid for inhibiting Ewing sarcoma cell growth.Investigational new drugs · 2017Article
- Induction of miR-137 by Isorhapontigenin (ISO) Directly Targets Sp1 Protein Translation and Mediates Its Anticancer Activity Both In Vitro and In Vivo.Molecular cancer therapeutics · 2016Article
- MicroRNA-Specificity Protein (Sp) Transcription Factor Interactions and Significance in Carcinogenesis.Current pharmacology reports · 2015Article
- Role of Brg1 in progression of esophageal squamous cell carcinoma.Iranian journal of basic medical sciences · 2014Article
- Anti-tumor activity of non-steroidal anti-inflammatory drugs: cyclooxygenase-independent targets.Cancer letters · 2014Review
- Article
- The involvement of endoplasmic reticulum stress in the suppression of colorectal tumorigenesis by tolfenamic acid.Cancer prevention research (Philadelphia, Pa.) · 2013Article
- Betulinic acid decreases ER-negative breast cancer cell growth in vitro and in vivo: role of Sp transcription factors and microRNA-27a:ZBTB10.Molecular carcinogenesis · 2013Article
- Apoptotic effect of tolfenamic acid on MDA-MB-231 breast cancer cells and xenograft tumors.Journal of clinical biochemistry and nutrition · 2013Article
- Inhibition of rhabdomyosarcoma cell and tumor growth by targeting specificity protein (Sp) transcription factors.International journal of cancer · 2013Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
The non-steroidal anti-inflammatory drug tolfenamic acid (TA) inhibits proliferation of SEG-1 and BIC-1 esophageal cancer cells with half-maximal growth inhibitory concentration values of 36 and 48 muM, respectively. TA also increased Annexin V staining in both cell lines, indicative of proapoptotic activity. Treatment of SEG-1 and BIC-1 cells with TA for up to 72 h decreased expression of specificity protein (Sp) transcription factors Sp1, Sp3 and Sp4 and this was accompanied by decreased expression of the well-characterized Sp-regulated genes cyclin D1, vascular endothelial growth factor and survivin. TA also decreased hepatocyte growth factor receptor, (c-Met), a receptor tyrosine kinase that is overexpressed in esophageal cancer cells and tumors and is an important drug target. Knockdown of Sp1, Sp3 and Sp4 by RNA interference in SEG-1 and BIC-1 cells also decreased c-Met expression, demonstrating that c-Met is an Sp-regulated gene in esophageal cancer cells. Sp1 was overexpressed in esophageal cancer cells and tumors and increased Sp1 staining was observed in esophageal tumors from patients. TA (20 mg/kg/day) also decreased tumor growth and weight in athymic nude mice bearing SEG-1 cells as xenografts and this was accompanied by increased apoptosis and decreased Sp1 and c-Met staining in tumors from treated mice. Thus, TA-dependent downregulation of Sp transcription factors and c-Met defines a novel chemotherapeutic approach for treatment of esophageal cancer.
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Registered trials
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