ABSTRACT
<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>
Subject(s)
Female , Humans , Male , Middle Aged , Cadherins , Metabolism , Carcinoma, Squamous Cell , Metabolism , Pathology , Cell Differentiation , Cytoskeletal Proteins , Metabolism , Esophageal Neoplasms , Metabolism , Pathology , Lymphatic Metastasis , Neoplasm InvasivenessABSTRACT
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.