ArticleWorld journal of gastroenterology2009
Effects of ciglitazone and troglitazone on the proliferation of human stomach cancer cells.
Article in World journal of gastroenterology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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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
16 citing papers in PubMed, 26 citations in OpenAlex.
- Stomach at the crossroads: nuclear receptor signaling at the interface between what we are and what we eat.Physiological reviews · 2026Review
- Mapping the Single-Cell Differentiation Landscape of Osteosarcoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024Article
- S100a9 might act as a modulator of the Toll-like receptor 4 transduction pathway in chronic rhinosinusitis with nasal polyps.Scientific reports · 2024Article
- Review
- Structural Biology-Based Exploration of Subtype-Selective Agonists for Peroxisome Proliferator-Activated Receptors.International journal of molecular sciences · 2021Review
- Article
- Peroxisome Proliferator Activated Receptor Gamma Sensitizes Non-small Cell Lung Carcinoma to Gamma Irradiation Induced Apoptosis.Frontiers in genetics · 2019Article
- IFRD1 polymorphisms and gastric cancer risk in a Chinese population.Medical oncology (Northwood, London, England) · 2014Article
- Alterations in lipid mediated signaling and Wnt/ β -catenin signaling in DMH induced colon cancer on supplementation of fish oil.BioMed research international · 2014Article
- Association of thiazolidinediones with gastric cancer in type 2 diabetes mellitus: a population-based case-control study.BMC cancer · 2013Article
- The Role of PPARγ in Helicobacter pylori Infection and Gastric Carcinogenesis.PPAR research · 2012Article
- The Role of PPARγ in the Transcriptional Control by Agonists and Antagonists.PPAR research · 2012Article
- Peroxisome proliferator-activated receptors and cancer: challenges and opportunities.British journal of pharmacology · 2011Review
- Induction of metastatic gastric cancer by peroxisome proliferator-activated receptorδ activation.PPAR research · 2010Article
- Gastrointestinal Cytoprotection by PPARγ Ligands.PPAR research · 2010Article
- Troglitazone reverses the multiple drug resistance phenotype in cancer cells.Drug design, development and therapy · 2009Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo determine the cytological and molecular effects of peroxisome proliferation-activated receptor (PPAR)-gamma and PPAR-gamma agonists on stomach cancer cells.
methodsTo determine the proliferation-suppressive effects of troglitazone and ciglitazone, SNU-216 and SNU-668 stomach cancer cells were plated in media containing 40 micromol/L troglitazone and ciglitazone at a density of 1 multiply 10(4) cells/well. After 3, 5 and 7 d, the cells were counted with a hemocytometer. To assess the appearance of PPAR-gamma, a reverse-transcription polymerase chain reaction analysis was performed. On day 7, Western blotting was used to determine the effects of troglitazone and ciglitazone on the expression of p21 and phosphorylated-ERK (pERK) genes. Flow cytometry analysis was used to determine which portion of the cell cycle was delayed when troglitazone was used to suppress cell proliferation. In order to clarify the mechanism underlying the activity of troglitazone, microarray analysis was conducted.
resultsPPAR-gamma was manifested in both SNU-216 and SNU-668 cells. Ciglitazone and troglitazone suppressed cell growth, and troglitazone was a stronger suppressor of stomach cancer cells than ciglitazone, an inducer of cell cycle arrest in the G1 phase. SNU-668 cells were also determined to be more sensitive to ciglitazone and troglitazone than SNU-216 cells. When troglitazone and ciglitazone were administered to stomach cancer cells, levels of p21 expression were increased, but ERK phosphorylation levels were reduced. When GW9662, an antagonist of PPAR-gamma, was applied in conjunction with ciglitazone and troglitazone, the cell growth suppression effect was unaffected. The gene transcription program revealed a variety of alterations as the consequence of troglitazone treatment, and multiple troglitazone-associated pathways were detected. The genes whose expression was increased by troglitazone treatment were associated with cell development, differentiation, signal transmission between cells, and cell adhesion, and were also associated with reductions in cell proliferation, the cell cycle, nuclear metabolism, and phosphorylation.
conclusionTroglitazone and ciglitazone suppress the proliferation of stomach cancer cells via a PPAR-gamma-independent pathway.
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