ABSTRACT
No abstract available.
ABSTRACT
El cáncer gástrico es una de las enfermedades neoplásicas de más alta incidencia y mortalidad a nivel mundial: es el segundo tipo de cáncer más frecuente en el mundo y la primera causa mundial de mortalidad por esta enfermedad. Por su parte, la apoptosis es un proceso importante de muerte celular programada que se presenta durante la embriogénesis, la regulación del sistema inmune y el mantenimiento de la homeostasis tisular. La evasión de la apoptosis por diferentes mecanismos es uno de los aspectos moleculares más importantes en el desarrollo de cáncer. En este artículo se presenta una revisión exhaustiva de la evidencia del papel de la apoptosis vía Fas/FasL en el desarrollo de la carcinogénesis gástrica, inclusive desde etapas tempranas, como la aparición de lesiones preneoplásicas. Finalmente, se evidencia que el desarrollo de más estudios permitiría esclarecer mejor el papel de la vía Fas/FasL en la carcinogénesis gástrica, en sus diferentes estadios.
Gastric cancer is an important neoplastic disease in all around the world because its high incidence and mortality. Otherwise, apoptosis is a key process of programmed cell death during embryogenesis, regulation of immune system, and holding the tissue homeostasis. Besides, the escape of apoptosis by different ways is an essential molecular aspect for the development of cancer. In this article we present an exhaustive review of the current evidence of the role of apoptosis through Fas/FasL pathway in the development of gastric carcinogenesis, including since early stages like in appearance of preneoplastic lesions. Finally, we think that a better comprehension of the signaling pathway Fas/ FasL role in the different stages of gastric carcinogenesis could let us know more about the implicated molecular ways and the physiopathological changes in the appearance of this disease.
Subject(s)
Humans , Stomach Neoplasms , Causality , Apoptosis , fas Receptor , Fas Ligand ProteinABSTRACT
PURPOSE: To identify the mechanism of azaline B-dependent apoptosis, the regulation of Fas and FasL genes has been investigated. MATERIALS AND METHODS: Azaline B was subcutaneously injected into Sprague-Dawley rats. The levels of Fas receptor (Fas) and Fas ligand (FasL) were detected by reverse transcription-polymerase chain reaction (RT- PCR). Azaline B-dependent apoptosis was determined by terminal deoxynucleotidyl transferase-mediated dUTP nick and labeling (TUNEL) and DNA fragmentation assay. Transacting factor of FasL promoter was identified by DNase I footprinting and DNA mobility shift assay. RESULTS: The azaline B-treated testis (250microgram/kg body wt/day) had decreased to 70+/-2.5% and 38+/-1.8% of the normal testis weight at 3 and 5 days after the injection, respectively, but the weights of the testis were not changed after pretreatment of follicle-stimulating hormone (FSH) and testosterone. Apoptosis of the testis was detected by DNA fragmentation assay and TUNEL assay after the azaline B treatment. The levels of Fas and FasL mRNA were increased by the treatment of azaline B in both time- and dose-dependent manners. In DNase I footprinting assay with FasL promoter, the nuclear factor prepared from control was bound with at least four sites: SP-1 binding site at 283, NF-kappa B binding site at 219, TATA at 132 and the gamma-interferon response element (gamma-IRE) at 78. gamma-IRE was completely protected by the nuclear extract prepared from azaline B-treated rat testis. In DNA mobility shift assay, the binding activity of gamma-IRE binding protein was increased after azaline B treatment. CONCLUSIONS: These results suggest that Fas-FasL system may be important to azaline B-dependent apoptosis in rat testis and that gamma-IRE binding protein is related to the azaline B-dependent regulation of FasL gene.
Subject(s)
Animals , Rats , fas Receptor , Apoptosis , Binding Sites , Carrier Proteins , Deoxyribonuclease I , DNA , DNA Fragmentation , Electrophoretic Mobility Shift Assay , Fas Ligand Protein , Follicle Stimulating Hormone , In Situ Nick-End Labeling , Interferon-gamma , NF-kappa B , Rats, Sprague-Dawley , Response Elements , RNA, Messenger , Testis , Testosterone , Weights and MeasuresABSTRACT
BACKGROUNDS: Castration-induced androgen deprivation triggers a sequence of events, which activates apoptotic cell death of the androgen-dependent epithelial cells within the rat ventral prostate. To investigate the mechanism of castration-dependent apoptosis in the rat ventral prostate, the regulation of apoptosis-related genes was been investigated. METHODS: Azaline B was subcutaneously injected into Sprague-Dawley rat. The Fas receptor (Fas), Fas ligand (FasL) and bcl-2 mRNA, as well as the protein levels were detected by RT-PCR and Western blot analyses. Azaline B-dependent apoptosis was determined using TUNEL and a DNA fragmentation assay. The transacting factor of the FasL promoter was identified by DNA footprinting and a DNA mobility shift assay. RESULTS: The rat prostate was regressed after castration, with and the involuted ventral prostate regenerated by testosterone pretreatment, but not by that with FSH. Apoptosis of the ventral prostate was detected, after castration, using toluidine blue staining, a TUNEL assay and an apoptotic DNA fragmentation assay. The levels of Fas, FasL mRNA and protein were increased after castration. In the DNase I footprinting assay, using the FasL promoter and a nuclear extract prepared from a control prostate, at least two sites were protected: the SP-1 binding site at -283 bp and the prostate-unidentified factor(P-UF) binding site at -247 bp. The SP-1 binding activity vanished in the nuclear extract prepared from castrated rats. In the DNA mobility shift assay, the SP-1 binding activity was slightly decreased after castration. Both the Bcl-2 mRNA and Bcl-2 protein were downregulated after castration. CONCLUSION: These results suggest that the Fas/FasL system and Bcl-2 may be important to castrationdependent apoptosis in the rat ventral prostate, with SP-1 related to the castration-dependent regulation of the FasL gene
Subject(s)
Animals , Rats , fas Receptor , Apoptosis , Binding Sites , Blotting, Western , Castration , Cell Death , Deoxyribonuclease I , DNA , DNA Footprinting , DNA Fragmentation , Electrophoretic Mobility Shift Assay , Epithelial Cells , Fas Ligand Protein , In Situ Nick-End Labeling , Prostate , Rats, Sprague-Dawley , RNA, Messenger , Testosterone , Tolonium ChlorideABSTRACT
BACKGROUNDS: Castration-induced androgen deprivation triggers a sequence of events, which activates apoptotic cell death of the androgen-dependent epithelial cells within the rat ventral prostate. To investigate the mechanism of castration-dependent apoptosis in the rat ventral prostate, the regulation of apoptosis-related genes was been investigated. METHODS: Azaline B was subcutaneously injected into Sprague-Dawley rat. The Fas receptor (Fas), Fas ligand (FasL) and bcl-2 mRNA, as well as the protein levels were detected by RT-PCR and Western blot analyses. Azaline B-dependent apoptosis was determined using TUNEL and a DNA fragmentation assay. The transacting factor of the FasL promoter was identified by DNA footprinting and a DNA mobility shift assay. RESULTS: The rat prostate was regressed after castration, with and the involuted ventral prostate regenerated by testosterone pretreatment, but not by that with FSH. Apoptosis of the ventral prostate was detected, after castration, using toluidine blue staining, a TUNEL assay and an apoptotic DNA fragmentation assay. The levels of Fas, FasL mRNA and protein were increased after castration. In the DNase I footprinting assay, using the FasL promoter and a nuclear extract prepared from a control prostate, at least two sites were protected: the SP-1 binding site at -283 bp and the prostate-unidentified factor(P-UF) binding site at -247 bp. The SP-1 binding activity vanished in the nuclear extract prepared from castrated rats. In the DNA mobility shift assay, the SP-1 binding activity was slightly decreased after castration. Both the Bcl-2 mRNA and Bcl-2 protein were downregulated after castration. CONCLUSION: These results suggest that the Fas/FasL system and Bcl-2 may be important to castrationdependent apoptosis in the rat ventral prostate, with SP-1 related to the castration-dependent regulation of the FasL gene
Subject(s)
Animals , Rats , fas Receptor , Apoptosis , Binding Sites , Blotting, Western , Castration , Cell Death , Deoxyribonuclease I , DNA , DNA Footprinting , DNA Fragmentation , Electrophoretic Mobility Shift Assay , Epithelial Cells , Fas Ligand Protein , In Situ Nick-End Labeling , Prostate , Rats, Sprague-Dawley , RNA, Messenger , Testosterone , Tolonium ChlorideABSTRACT
PURPOSE: Androgen deprivation triggers a sequence of events that activates apoptotic cell death of the androgen-dependent epithelial cells within the rat ventral prostate, ultimately resulting in the involution of the gland. To investigate the mechanism of azaline B-dependent apoptosis in the rat ventral prostate, the regulation of apoptosis-related genes were examined. MATERIALS AND METHODS: Azaline B was subcutaneously injected in Sprague-Dawley rat. Fas receptor(Fas), Fas ligand(FasL), bcl-2 mRNA, and protein levels were detected by RT-PCR and Western blot. Azaline B-dependent apoptosis was determined by TUNEL and DNA fragmentation assay. Transacting factor of FasL promoter was identified by DNA footprinting and DNA mobility shift assay. RESULTS: The prostate regressed after azaline B treatment in rat, and the involuted ventral prostate regenerated after testosterone pretreatment. Apoptosis of the ventral prostate was detected by TUNEL assay and apoptotic DNA fragmentation assay after azaline B treatment. The levels of Fas and FasL mRNA and protein increased after azaline B treatment. In DNase I footprinting assay with FasL promoter using nuclear extract prepared from control prostate, at least two sites were protected: SP-1 binding site at -283bp and prostate-unidentified factor(P-UF) binding site at -247bp. SP-1 binding activity vanished in the nuclear extract prepared from azaline B-treated rats. In the DNA mobility shift assay, SP-1 binding activity decreased after azaline B treatment. Bcl-2 mRNA and protein were downregulated after azaline B treatment. CONCLUSIONS: These results suggest that Fas/FasL system and Bcl-2 are important to azaline B-dependent apoptosis in rat ventral prostate and that SP-1 is related to azaline B-dependent regulation of the FasL gene.
Subject(s)
Animals , Rats , fas Receptor , Apoptosis , Binding Sites , Blotting, Western , Cell Death , Deoxyribonuclease I , DNA , DNA Footprinting , DNA Fragmentation , Electrophoretic Mobility Shift Assay , Epithelial Cells , Fas Ligand Protein , Genes, bcl-2 , In Situ Nick-End Labeling , Prostate , Rats, Sprague-Dawley , RNA, Messenger , TestosteroneABSTRACT
Objective To discuss the variation range and the indication of soluble serum Fas (sFas) in aplastic anemia (AA) patients.Methods The level of sFas receptor in 38 AA patients was assayed by ELISA,with 30 cases as controls.Results The level of sFas receptor in AA patients was apparently lower than those of the control group (P
ABSTRACT
No abstract available.
ABSTRACT
To detect the soluble Fas (sFas) receptor level in sera from patients with myelodysplastic syndrome (MDS) and acute leukemia (AL), and investigate its clinical significance, the levels of sFas receptor in sera from 18 patients with MDS and 42 patients with AL were detected by using ELISA methods. The results suggested that the sFas receptor levels in sera from patients with MDS-RA were significantly lower than that from normal control (2.89?1.72 ng/ml vs 6.29?1.07 ng/ml, P
ABSTRACT
0. 05 ]. However, the level of sFas was significantly higher in the patients with CHF than those of the cardiac function class Ⅰ group [CHF group: 1353. 30 ? 507. 71 (cardiac function class Ⅱ 1154. 85 ? 371.20, class Ⅲ 1412. 88 ? 493. 62, class Ⅳ 1875.67 ? 806. 10) vs. cardiac function class Ⅰ group:983. 11 ? 416.26 pg/ml, P