ABSTRACT
<p><b>OBJECTIVE</b>To study expression of MMP-2 in relation to microvessel density (MVD) in esophageal carcinoma.</p><p><b>METHODS</b>Forty-eight specimens of esophageal carcinoma (Ec) and 17 specimens of grade II + III epithelial dysplasia (Dy) close to the tumor and 12 specimens of normal tissue (Nt) along the incisional margin were examined by S-P immunohistochemical staining with anti-MMP-2 monoclonal antibody. An anti-CD34 monoclonal antibody was used to show MVD.</p><p><b>RESULTS</b>MMP-2 expression in Ec was remarkably higher than that in Dy, which was higher than that in Nt. MMP-2 expression in Ec and Dy was significantly correlated with MVD in the tumor and nearby tissue. MMP-2 expression and MVD in Ec significantly associated with lymph node metastasis.</p><p><b>CONCLUSION</b>Expression of MMP-2 plays an important role in angiogenesis and lymph node metastasis of esophageal cancer.</p>
Subject(s)
Female , Humans , Male , Middle Aged , Carcinoma, Squamous Cell , Esophageal Neoplasms , Pathology , Lymphatic Metastasis , Matrix Metalloproteinase 2 , Metabolism , Microcirculation , Pathology , Neovascularization, Pathologic , PathologyABSTRACT
<p><b>OBJECTIVE</b>To investigate the effects of ginsenoside Rh2 (GS-Rh2) on growth inhibition and cell cycle of Eca-109 esophageal carcinoma cell line in culture.</p><p><b>METHOD</b>The effects of GS-Rh2 on cell growth inhibition was detected by MTT assay. Cell cycle was analyzed by flow cytometry (FCM). Cell morphology was observed by a light microscope after HE staining. The protein expression of cell cycle components (cyclinE, CDK2, p21WAF1) were examined by immunocytochemistry and Western blot. The mRNA expression were examined by semiquantitative RT-PCR.</p><p><b>RESULT</b>GS-Rh2 inhibited the proliferation of Eca-109 cells in dose and time-dependent manners. The inhibition rate was about 50% after 1-day treatment with 20 microg x mL(-1) GS-Rh2 x 20 microg x mL(-1) GS-Rh2 induced the mature differentiation and morphological reversion. With increasing dose of GS-Rh2 treatment, the cell number of G0/G1 phase was increased, whereas it decreased at S and G2/M phase. There was significant difference between 10, 20 microg x mL(-1) GS-Rh2 groups and the corresponding group without GS-Rh2 treatement. After treating cells by 20 microg x mL(-1) GS-Rh2 for 1, 2, 3 days individually, the protein and mRNA expression of both cyclinE and CDK2 reduced, while the expression of p21WAF1 enhanced gradually.</p><p><b>CONCLUSION</b>GS-Rh2 could arrest Eca-109 cells at G0/G1 phase and induce cell differentiation tending to normal. Furthermore, GS-Rh2 had an effect on expression of cell cycle components (cyclinE, CDK2 and p21WAF1) to inhibit Eca-109 cell proliferation.</p>