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1.
Rev. bras. pesqui. méd. biol ; Braz. j. med. biol. res;48(3): 226-233, 03/2015. graf
Article in English | LILACS | ID: lil-741251

ABSTRACT

Peroxisome proliferator activator receptor-gamma (PPARγ) is a ligand-activated transcriptional factor involved in the carcinogenesis of various cancers. Insulin-like growth factor-binding protein-3 (IGFBP-3) is a tumor suppressor gene that has anti-apoptotic activity. The purpose of this study was to investigate the anticancer mechanism of PPARγ with respect to IGFBP-3. PPARγ was overexpressed in SNU-668 gastric cancer cells using an adenovirus gene transfer system. The cells in which PPARγ was overexpressed exhibited growth inhibition, induction of apoptosis, and a significant increase in IGFBP-3 expression. We investigated the underlying molecular mechanisms of PPARγ in SNU-668 cells using an IGFBP-3 promoter/luciferase reporter system. Luciferase activity was increased up to 15-fold in PPARγ transfected cells, suggesting that PPARγ may directly interact with IGFBP-3 promoter to induce its expression. Deletion analysis of the IGFBP-3 promoter showed that luciferase activity was markedly reduced in cells without putative p53-binding sites (-Δ1755, -Δ1795). This suggests that the critical PPARγ-response region is located within the p53-binding region of the IGFBP-3 promoter. We further demonstrated an increase in PPARγ-induced luciferase activity even in cells treated with siRNA to silence p53 expression. Taken together, these data suggest that PPARγ exhibits its anticancer effect by increasing IGFBP-3 expression, and that IGFBP-3 is a significant tumor suppressor.


Subject(s)
Adult , Female , Humans , Male , Asthma/chemically induced , Genes, MHC Class I/genetics , Genes, MHC Class II/genetics , Isocyanates/toxicity , Occupational Diseases/chemically induced , Occupational Exposure/adverse effects , Asthma/genetics , Genetic Variation , Genotype , Occupational Diseases/genetics , Polymorphism, Single Nucleotide , Risk
2.
Braz J Med Biol Res ; 48(3): 226-33, 2015 Mar.
Article in English | MEDLINE | ID: mdl-25590353

ABSTRACT

Peroxisome proliferator activator receptor-gamma (PPARγ) is a ligand-activated transcriptional factor involved in the carcinogenesis of various cancers. Insulin-like growth factor-binding protein-3 (IGFBP-3) is a tumor suppressor gene that has anti-apoptotic activity. The purpose of this study was to investigate the anticancer mechanism of PPARγ with respect to IGFBP-3. PPARγ was overexpressed in SNU-668 gastric cancer cells using an adenovirus gene transfer system. The cells in which PPARγ was overexpressed exhibited growth inhibition, induction of apoptosis, and a significant increase in IGFBP-3 expression. We investigated the underlying molecular mechanisms of PPARγ in SNU-668 cells using an IGFBP-3 promoter/luciferase reporter system. Luciferase activity was increased up to 15-fold in PPARγ transfected cells, suggesting that PPARγ may directly interact with IGFBP-3 promoter to induce its expression. Deletion analysis of the IGFBP-3 promoter showed that luciferase activity was markedly reduced in cells without putative p53-binding sites (-Δ1755, -Δ1795). This suggests that the critical PPARγ-response region is located within the p53-binding region of the IGFBP-3 promoter. We further demonstrated an increase in PPARγ-induced luciferase activity even in cells treated with siRNA to silence p53 expression. Taken together, these data suggest that PPARγ exhibits its anticancer effect by increasing IGFBP-3 expression, and that IGFBP-3 is a significant tumor suppressor.


Subject(s)
Apoptosis/drug effects , Insulin-Like Growth Factor Binding Protein 3/metabolism , PPAR gamma/metabolism , Stomach Neoplasms/pathology , Cell Line, Tumor , Gene Expression Regulation, Neoplastic/drug effects , Humans , Insulin-Like Growth Factor Binding Protein 3/genetics , PPAR gamma/genetics , Signal Transduction , Stomach Neoplasms/metabolism , Transcriptional Activation , Up-Regulation
3.
Br J Rheumatol ; 32(8): 663-5, Aug. 1993.
Article in English | MedCarib | ID: med-8471

ABSTRACT

We report a significantly increased prevalence of antribosomal P protein antibodies in Malaysian Chinese patients (38 percent) with SLE compared to white caucasian (13 percent) and Afro-Caribbean (20 percent) patients. The increase prevalence was not due to a generalized increase in autoantibody production because anti-dsDNA and anti-SSA antibodies were present in comparable frequencies in the three ethnic groups while anti-Sm and anti-SSB antibodies were rarely found in the Malaysian Chinese patients (AU)


Subject(s)
Humans , Antibodies, Anti-Idiotypic/analysis , Antibodies, Bacterial/analysis , Lupus Erythematosus, Systemic/immunology , Ribosomal Proteins/immunology , Lupus Erythematosus, Systemic/blood , Lupus Erythematosus, Systemic/genetics
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