ArticleEuropean journal of pharmacology2010
MCC-555-induced NAG-1 expression is mediated in part by KLF4.
Article in European journal of pharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 16 citations in OpenAlex.
- Mutations of p53 decrease sensitivity to the anthracycline treatments in bladder cancer cells.Oncotarget · 2018Article
- CRP Stimulates GDF15 Expression in Endothelial Cells through p53.Mediators of inflammation · 2018Article
- Ethanol-induced changes in poly (ADP ribose) polymerase and neuronal developmental gene expression.Neuropharmacology · 2016Article
- Nuclear receptors and pathogenesis of pancreatic cancer.World journal of gastroenterology · 2014Review
- Peroxisome proliferator-activated receptor γ agonists induce cell cycle arrest through transcriptional regulation of Kruppel-like factor 4 (KLF4).The Journal of biological chemistry · 2013Article
- CDX2-driven leukemogenesis involves KLF4 repression and deregulated PPARγ signaling.The Journal of clinical investigation · 2013Article
- A peroxisome proliferator-activated receptor ligand MCC-555 imparts anti-proliferative response in pancreatic cancer cells by PPARgamma-independent up-regulation of KLF4.Toxicology and applied pharmacology · 2012Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Peroxisome proliferator-activated receptor gamma (PPARgamma) plays a central role in cell differentiation, metabolism and tumorigenesis. We have investigated the therapeutic properties of 5-[[6-[(2-fluorophenyl)-methoxy]-2-napthalenyl]-methyl]-2,4-thiazolidinedione (MCC-555) a PPARgamma agonist in human colorectal cancer cells. To elucidate the molecular mechanism(s), by which MCC-555 exerts its effects on the human colorectal cancer cells, we have analyzed the expression of two pro-apoptotic proteins, Krüppel-like factor 4 (KLF4) and nonsteroidal anti-inflammatory drug (NSAID)-activated gene-1 (NAG-1). MCC-555-induced expression of the transcription factor, KLF-4 was blocked by a PPARgamma specific antagonist GW9662 in PPARgamma-dependent manner in HCT-116 cells. We further identified a new KLF4 target gene NAG-1, which shows a pro-apoptotic activity. We confirmed that PPARgamma agonists-induced NAG-1 expression was abolished using KLF4 siRNA in HCT-116 cells. Subsequently, KLF4 expression enhances the NAG-1 promoter activity in HCT-116 cells, and functional KLF4 binding sites in the NAG-1 promoter were also identified. MCC-555, a PPARgamma agonist induced the expression of Klf4 mRNA and protein in murine intestinal tumors from MCC-555-treated mice, as assessed by RT-PCR and immunohistochemistry. This study shows that PPARgamma agonists up-regulate KLF4 expression in receptor-dependent manner, and KLF4 was identified as a novel transcription factor that controls NAG-1 promoter activity in human and mouse colorectal cancers.
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