RESUMEN
<p><b>BACKGROUND AND OBJECTIVE</b>It has been proven that Ezrin protein may interact with E-cadherin protein and take part in metastasis of tumor cells. This study was to investigate the expressions of Ezrin and E-cadherin in esophageal squamous cell carcinoma (ESCC) and their relationship with the clinicopathologic factors, and analyze their diagnostic values for ESCC.</p><p><b>METHODS</b>The expression of Ezrin and E-cadherin in 72 specimen of ESCC and the paracancer normal squamous epithelium was detected using tissue array with SP immunohistochemistry. Their correlations to the clinicopathologic factors were analyzed statistically.</p><p><b>RESULTS</b>The positive rate of Ezrin was significantly higher in ESCC than in para-cancer normal squamous epithelium (90.7% vs. 46.0%, P < 0.001); the positive rate of E-cadherin was significantly lower in ESCC than in para-cancer normal squamous epithelium (27.6% vs. 97.4%, P < 0.001). Ezrin expression was related to the invasiveness and lymph node metastasis of ESCC (P < 0.05); E-cadherin expression was related to the differentiation and lymph node metastasis of ESCC (P < 0.05). The high expression of Ezrin was related to the low expression of E-cadherin (P < 0.05).</p><p><b>CONCLUSION</b>The activation of Ezrin and the absence of E-cadherin contribute to the tumorigenesis and metastasis of ESCC.</p>
Asunto(s)
Femenino , Humanos , Masculino , Persona de Mediana Edad , Cadherinas , Metabolismo , Carcinoma de Células Escamosas , Metabolismo , Patología , Diferenciación Celular , Proteínas del Citoesqueleto , Metabolismo , Neoplasias Esofágicas , Metabolismo , Patología , Metástasis Linfática , Invasividad NeoplásicaRESUMEN
The aim of this study was to clarify whether bortezomib might induce apoptosis in Burkitt's lymphoma Raji cell line and its mechanism. Different concentrations of bortezomib were used to treat Raji cells and its effects of time and dose were observed. Cell morphology was observed under light microscope; flow cytometry was used to analyze cell apoptosis; RT-PCR was used to detect the expressions of NF-kappaB and p53 gene mRNAs. The results showed that the bortezomib could inhibit Raji cell growth within a certain range of treating time and dose. Apoptosis were induced in relation to time and dose. The expression of NF-kappaB mRNA and p53 mRNA decreased after treatment with bortezomib. It is concluded that the bortezomib can induce Raji cell apoptosis, which provides a theoretical basis for clinical treatment. NF-kappaB and p53 gene are supposed to participate in the bortezomib induced apoptosis of Raji cells.
Asunto(s)
Humanos , Apoptosis , Ácidos Borónicos , Farmacología , Bortezomib , Linfoma de Burkitt , Metabolismo , Patología , Línea Celular Tumoral , Proliferación Celular , Citometría de Flujo , FN-kappa B , Metabolismo , Pirazinas , Farmacología , Proteína p53 Supresora de Tumor , MetabolismoRESUMEN
Objective To establish the mouse models of acute epilepsy induced by kainic acid or penicillin, and explore the characteristics and condition of application of the 2 agents. Methods Ninety healthy male Kunming mice were selected and divided randomly into the normal saline group (n=10) and penicillin-induced group (n=40) and kainic acid-induced group (n=40). The kainic acid-induced group were treated with 10 mg/kg kainic acid by intraperitoneal injection, the penicillin-induced group were treated with 7× 106 U/kg penicillin by intraperitoneal injection, and the ones in the normal saline group were treated with 35 μL/g normal saline by intraperitoneal injection. After injection, seizure was observed continuously and graded in the following 5 h and monitored by electroencephalogram (EEG). Results Totally 80 mice of the penicillin- and kainic acid-induced groups entered the final analysis. It was noted that the latency of the appearance of the status epilepticus by kainic acid was shorter than that by penicillin (P<0.05), and the mortality rate was lower as well (P<0.05). Conclusions Acute epilepsy model reproduced by kainic acid might be superior to the one by penicillin because of the similar behavior and EEG features with human temporal epilepsy.