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1.
Rev. bras. pesqui. méd. biol ; Braz. j. med. biol. res;52(1): e7816, 2019. tab, graf
Artículo en Inglés | LILACS | ID: biblio-974271

RESUMEN

Fibroblast growth factor receptor 1 (FGFR1) has been reported in gastric cancer to be a prognostic factor. However, miR-497-targeted FGFR1 has not been explored in the carcinogenesis of gastric cancer. The present study intended to revalidate the prognostic significance of FGFR1 in patients with gastric cancer, and the mechanism of miR-497-regulated FGFR1 was investigated in gastric cancer cell proliferation and apoptosis. The messenger RNA (mRNA) and protein levels were assayed by RT-qPCR and western blotting, respectively. The targeted genes were predicted by a bioinformatics algorithm and confirmed by a dual luciferase reporter assay. Cell proliferation was analyzed by CCK-8 assay. Annexin V-FITC/PI staining was used to evaluate the apoptosis in AGS and SGC-7901 cells. FGFR1 was frequently up-regulated in gastric cancer tissues and associated with poor overall survival in patients with gastric cancer. Interestingly, FGFR1 loss-of-function resulted in a significant growth inhibition and apoptosis in AGS and SGC-7901 cells. In addition, we found that miR-497 was inhibited in gastric cancer tissues and cell lines, while overexpression of miR-497 could suppress proliferation and induce apoptosis in AGS and SGC-7901 cells. Importantly, bioinformatics analysis and experimental data suggested that FGFR1 was a direct target of miR-497, which could inhibit FGFR1 expression when transfected with miR-497 mimics. Furthermore, we found that overexpression of FGFR1 reversed the growth inhibition and apoptosis of miR-497 mimics in AGS and SGC-7901 cells. These findings suggested that overexpression of miR-497 inhibited proliferation and induced apoptosis in gastric cancer through the suppression of FGFR1.


Asunto(s)
Humanos , Neoplasias Gástricas/genética , Regulación Neoplásica de la Expresión Génica , MicroARNs/metabolismo , Receptor Tipo 1 de Factor de Crecimiento de Fibroblastos/genética , Pronóstico , Neoplasias Gástricas/metabolismo , Neoplasias Gástricas/patología , ARN Mensajero/genética , ARN Mensajero/metabolismo , Inmunohistoquímica , Transducción de Señal , Western Blotting , Apoptosis , Progresión de la Enfermedad , Línea Celular Tumoral , Proliferación Celular , Receptor Tipo 1 de Factor de Crecimiento de Fibroblastos/metabolismo , Reacción en Cadena en Tiempo Real de la Polimerasa
2.
Braz J Med Biol Res ; 52(1): e7816, 2018 Nov 23.
Artículo en Inglés | MEDLINE | ID: mdl-30484492

RESUMEN

Fibroblast growth factor receptor 1 (FGFR1) has been reported in gastric cancer to be a prognostic factor. However, miR-497-targeted FGFR1 has not been explored in the carcinogenesis of gastric cancer. The present study intended to revalidate the prognostic significance of FGFR1 in patients with gastric cancer, and the mechanism of miR-497-regulated FGFR1 was investigated in gastric cancer cell proliferation and apoptosis. The messenger RNA (mRNA) and protein levels were assayed by RT-qPCR and western blotting, respectively. The targeted genes were predicted by a bioinformatics algorithm and confirmed by a dual luciferase reporter assay. Cell proliferation was analyzed by CCK-8 assay. Annexin V-FITC/PI staining was used to evaluate the apoptosis in AGS and SGC-7901 cells. FGFR1 was frequently up-regulated in gastric cancer tissues and associated with poor overall survival in patients with gastric cancer. Interestingly, FGFR1 loss-of-function resulted in a significant growth inhibition and apoptosis in AGS and SGC-7901 cells. In addition, we found that miR-497 was inhibited in gastric cancer tissues and cell lines, while overexpression of miR-497 could suppress proliferation and induce apoptosis in AGS and SGC-7901 cells. Importantly, bioinformatics analysis and experimental data suggested that FGFR1 was a direct target of miR-497, which could inhibit FGFR1 expression when transfected with miR-497 mimics. Furthermore, we found that overexpression of FGFR1 reversed the growth inhibition and apoptosis of miR-497 mimics in AGS and SGC-7901 cells. These findings suggested that overexpression of miR-497 inhibited proliferation and induced apoptosis in gastric cancer through the suppression of FGFR1.


Asunto(s)
Regulación Neoplásica de la Expresión Génica , MicroARNs/metabolismo , Receptor Tipo 1 de Factor de Crecimiento de Fibroblastos/genética , Neoplasias Gástricas/genética , Apoptosis , Western Blotting , Línea Celular Tumoral , Proliferación Celular , Progresión de la Enfermedad , Humanos , Inmunohistoquímica , Pronóstico , ARN Mensajero/genética , ARN Mensajero/metabolismo , Reacción en Cadena en Tiempo Real de la Polimerasa , Receptor Tipo 1 de Factor de Crecimiento de Fibroblastos/metabolismo , Transducción de Señal , Neoplasias Gástricas/metabolismo , Neoplasias Gástricas/patología
3.
Medicine (Baltimore) ; 96(20): e6949, 2017 May.
Artículo en Inglés | MEDLINE | ID: mdl-28514315

RESUMEN

Hepatic cirrhosis is often accompanied by functional kidney impairment, which may be reversed if early treatment is promptly administered. This study aimed to investigate the role of Cystatin C and Cystatin C estimated glomerular filtration rate in the diagnosis of kidney impairment in patients with hepatic cirrhosis.Four hundred sixty five patients with hepatic cirrhosis were recruited. Serum creatinine and Cystatin C were determined, and their estimated glomerular filtration rates were calculated.The area under the receiver-operating characteristic curve (area under curve [AUC]) of Cystatin C and Cystatin C estimated glomerular filtration rate was significantly larger than that of serum creatinine and serum creatinine estimated glomerular filtration rate, respectively (P = .000). When the optimal cut-off value and upper reference limit were used, similar sensitivity, misdiagnosis rate, and diagnostic consistency were only observed in Cystatin C estimated glomerular filtration rate (P > .05).Cystatin C and Cystatin C estimated glomerular filtration rate are superior to serum creatinine and serum creatinine estimated glomerular filtration rate in diagnosis of secondary kidney impairment, and Cystatin C estimated glomerular filtration rate has a better performance as compared with Cystatin C. However, it is not a measured parameter, and thus the lab should determine its own optimal cut-off value.


Asunto(s)
Cistatina C/sangre , Tasa de Filtración Glomerular , Cirrosis Hepática/complicaciones , Insuficiencia Renal/etiología , Insuficiencia Renal/metabolismo , Adulto , Anciano , Anciano de 80 o más Años , Área Bajo la Curva , Biomarcadores/metabolismo , Creatinina/sangre , Errores Diagnósticos , Femenino , Humanos , Cirrosis Hepática/metabolismo , Masculino , Persona de Mediana Edad , Curva ROC , Adulto Joven
4.
PLoS One ; 10(3): e0119385, 2015.
Artículo en Inglés | MEDLINE | ID: mdl-25790262

RESUMEN

The aims of this study were to simultaneously evaluate the expression of Y-box binding protein-1 (YB-1) in non-neoplastic rectal tissue and rectal cancer tissue, and to collect clinical follow-up data for individual patients. Additionally, we aimed to investigate the developmental functions and prognostic value of YB-1 in rectal cancer. We performed immunohistochemical studies to examine YB-1 expression in tissue samples from 80 patients with rectal cancer, 30 patients with rectal tubular adenoma, and 30 patients with rectitis. The mean YB-1 histological scores for rectal cancer, rectal tubular adenoma, and rectitis tissue specimens were 205.5, 164.3, and 137.7, respectively. Shorter disease-free and overall survival times were found in patients with rectal cancer who had higher YB-1 expression than in those with lower expression (38.2 months vs. 52.4 months, P = 0.013; and 44.4 months vs. 57.3 months, P = 0.008, respectively). Our results indicate that YB-1 expression is higher in rectal cancer tissue than in rectal tubular adenoma and rectitis tissue and that it may be an independent prognostic factor for rectal cancer.


Asunto(s)
Adenoma/genética , Biomarcadores de Tumor/biosíntesis , Neoplasias del Recto/genética , Proteína 1 de Unión a la Caja Y/biosíntesis , Adenoma/patología , Anciano , Biomarcadores de Tumor/genética , Supervivencia sin Enfermedad , Femenino , Regulación Neoplásica de la Expresión Génica , Humanos , Masculino , Persona de Mediana Edad , Estadificación de Neoplasias , Pronóstico , Neoplasias del Recto/patología , Proteína 1 de Unión a la Caja Y/genética
5.
Med Oncol ; 27(2): 219-23, 2010 Jun.
Artículo en Inglés | MEDLINE | ID: mdl-19291429

RESUMEN

Expression of the Raf kinase inhibitor protein (RKIP), a metastasis suppressor, is high in normal tissues, low in primary cancers, and lowest or absent in metastatic cancers. Here, we studied the expression of RKIP in nonneoplastic gastric tissue and gastric cancer tissue by immunohistochemistry (IHC) and evaluated its role in the genesis and metastasis of gastric cancer. RKIP immunoreactivity was evaluated in 40 samples of nonneoplastic gastric tissues and 75 samples of gastric cancer tissues. Among the 40 samples of nonneoplastic gastric tissue, 35 (87.5%) were positive for RKIP expression and 5 (12.5%) were negative; in the 75 samples of primary gastric cancer tissue, 39 (52%) were positive for RKIP expression and 36 (48%) were negative. Among 26 samples of metastatic lymph node tissues, 5 (19.2%) were positive for RKIP expression and 21 (80.8%) were negative. RKIP expression level was highest in nonneoplastic gastric tissue, low in primary gastric cancer tissue, and lowest or undetectable in metastatic gastric cancer tissue. Our data suggest that RKIP may play a role in the genesis and metastasis of gastric cancer.


Asunto(s)
Biomarcadores de Tumor/biosíntesis , Mucosa Gástrica/metabolismo , Proteínas de Unión a Fosfatidiletanolamina/biosíntesis , Neoplasias Gástricas/metabolismo , Mucosa Gástrica/enzimología , Gastroenteritis/diagnóstico , Gastroenteritis/metabolismo , Humanos , Inmunohistoquímica , Proteínas de Unión a Fosfatidiletanolamina/análisis , Neoplasias Gástricas/diagnóstico , Neoplasias Gástricas/enzimología
6.
Zhonghua Zhong Liu Za Zhi ; 25(5): 461-3, 2003 Sep.
Artículo en Chino | MEDLINE | ID: mdl-14575570

RESUMEN

OBJECTIVE: To study the prognostic identification of lymph node negative breast carcinoma by quantitative pathologic technique. METHODS: Several morphometrical parameters, DNA content of cell nuclei were detected by means of a quantitative pathologic technique on 102 patients with lymph node negative invasive breast duct carcinoma. The effects of potential prognostic factors of lymph node negative breast cancer patients were assessed by Cox's proportional hazards regression model. RESULTS: DNA index, minimal diameter of nuclei, area of nuclei, maximal diameter of nuclei, and the perimeter of nuclei are important factors to influence the prognosis. CONCLUSION: Quantitative pathologic technique combined with valid statistical methods, as an objective means of assessing prognosis, may reliably improve the outcome in lymph node negative breast cancer.


Asunto(s)
Neoplasias de la Mama/patología , Adulto , Anciano , ADN de Neoplasias/análisis , Femenino , Humanos , Metástasis Linfática , Persona de Mediana Edad , Análisis Multivariante , Pronóstico
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