ABSTRACT
<p><b>OBJECTIVE</b>To investigate the expression of EphA2 and EphrinA1 and its relationship with angiogenesis in renal cell carcinoma and its relevance to clinicopathologic features.</p><p><b>METHODS</b>The expression of the EphA2 and EphrinA1 was detected by immunohistochemistry (IHC) in the tissues samples from 68 renal cell carcinomas and 24 normal kidneys, and quantitatively analyzed. The microvessel density (MVD) was determined by CD34 immunostaining of microvascular endothelial cells. Statistical analysis was performed using the software SPSS (version 13.0).</p><p><b>RESULTS</b>The expression of EphA2, EphrinA1 and MND in the cancerous tissues were significantly higher (P<0.01) than that in the normal ones. Significantly increased expression of EphA2, EphrinA1 and MVD (P<0.01) was detected in cancer tissues with higher grade differentiation, more advanced stage and more lymph node metastasis, respectively (P<0.05 for each group). Expression of the EphA2 and EphrinA1 protein was shown to be positively associated with the MVD assessed by Spearman's correlation and factor analysis (r=0.555, r=0.485, P<0.01). The MVD was also significantly correlated with the diameter of the tumor (P<0.01).</p><p><b>CONCLUSION</b>EphA2 and EphrinA1 are highly expressed in renal cell carcinoma, and positively correlated with histological differentiation, clinical stage and angiogenesis in the cancer.</p>
Subject(s)
Adult , Aged , Aged, 80 and over , Female , Humans , Male , Middle Aged , Young Adult , Carcinoma, Renal Cell , Metabolism , Pathology , Ephrin-A1 , Metabolism , Kidney Neoplasms , Metabolism , Pathology , Lymphatic Metastasis , Microvessels , Pathology , Neoplasm Staging , Neovascularization, Pathologic , Metabolism , Pathology , Receptor, EphA2 , Metabolism , Tumor BurdenABSTRACT
Matrix metalloproteinases (MMPs) may contribute to the development of endometriosis. The aim of this study was to assess the effects of the polymorphisms in the promoters of MMP-7 (181A/G) and MMP-9 (1562C/T) on the risk of occurrence of endometriosis and adenomyosis. We genotyped 219 patients (143 women with endometriosis, 76 women with adenomyosis) and 160 control women in North China. There was a significant difference in frequency of the MMP-7 genotype between endometriosis and controls (P = 0.01) and also between adenomyosis and controls (P = 0.01). The frequency of the G allele in two groups of patients (7.3 and 7.9%) was significantly higher than in the controls (2.8%) (P = 0.01 and 0.01, respectively). Compared to the A/A genotype, the genotype with the -181G allele showed a significantly increased susceptibility to both diseases, with adjusted odds ratio of 2.62 [95% confidence interval (CI) = 1.17-5.87] for endometriosis and 3.14 (95% CI = 1.26-7.81) for adenomyosis. However, the overall genotype and allelotype distribution of the MMP-9 in the two case groups were not different from that of controls. We conclude that MMP-7-181A/G polymorphism has a potential to be a susceptibility factor for endometriosis and adenomyosis while MMP-9-1562C/T polymorphism may not provide a useful marker to predict susceptibility to endometriosis and adenomyosis, at least in women from North China.
Subject(s)
Endometriosis/genetics , Genetic Predisposition to Disease , Matrix Metalloproteinase 7/genetics , Matrix Metalloproteinase 9/genetics , Polymorphism, Single Nucleotide , Adult , China , Endometriosis/enzymology , Female , Humans , Middle Aged , Promoter Regions, GeneticABSTRACT
normal ovarian group (P
ABSTRACT
<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>
Subject(s)
Humans , Carcinoma, Squamous Cell , Pathology , Cell Cycle , Cell Line, Tumor , Cell Proliferation , Cyclin E , Genetics , Cyclin-Dependent Kinase 2 , Genetics , Cyclin-Dependent Kinase Inhibitor p21 , Genetics , Dose-Response Relationship, Drug , Drugs, Chinese Herbal , Pharmacology , Esophageal Neoplasms , Metabolism , Pathology , Ginsenosides , Pharmacology , Panax , Chemistry , Plants, Medicinal , Chemistry , RNA, Messenger , Genetics , Time FactorsABSTRACT
<p><b>OBJECTIVE</b>To study the expression and significance of cyclin E, cyclin D1, CDK4 and p27 protein in esophageal squamous cell cancer (ESCC) and their correlation with tumor differentiation and lymph node metastasis.</p><p><b>METHODS</b>Expressions of cyclin E, cyclin D1, CDK4 and p27 protein in 65 patients with ESCC were quantitatively detected by flow cytometry.</p><p><b>RESULTS</b>The expressions of cyclin E, cyclin D1, CDK4 in poorly-differentiated ESCC were higher than those in well-differentiated ESCC (P = 0.0275, 0.0001, 0.0174). The expression of p27 in poorly-differentiated ESCC was lower than that in well-differentiated ESCC (P = 0.0042). There was positive correlation between cyclin E and cyclin D1, cyclin D1 and CDK4, but negative correlation between cyclin D1 and p27. The expressions of all four proteins were not correlated with lymph node metastasis.</p><p><b>CONCLUSION</b>The expressions of cyclin E, cyclin D1, CDK4 and p27 are closely related to tumor differentiation of ESCC. An imbalance between positive and negative control of cell cycling might be critical in the carcinogenesis of esophageal squamous cell cancer.</p>
Subject(s)
Adult , Aged , Female , Humans , Male , Middle Aged , Carcinoma, Squamous Cell , Metabolism , Cell Differentiation , Cyclin D1 , Metabolism , Cyclin E , Metabolism , Cyclin-Dependent Kinase 4 , Metabolism , Cyclin-Dependent Kinase Inhibitor p27 , Metabolism , Cyclins , Metabolism , Esophageal Neoplasms , Metabolism , Pathology , Flow Cytometry , Lymph Nodes , Pathology , Lymphatic MetastasisABSTRACT
<p><b>OBJECTIVE</b>To explore the effects of Sterigmatocystin (ST), Deoxynivalenol (DON) and Aflatoxin G1 (AFG1) on apoptosis of human peripheral blood lymphocytes (HPBLs) in vitro and thus to further elucidate the putative roles of these three mycotoxins on human immunosystem.</p><p><b>METHODS</b>The effects of ST, DON and AFG1 on apoptosis of HPBLs were studied with cell culture, flow cytometric (FCM) DNA analysis and DNA agarose gel electrophoresis.</p><p><b>RESULTS</b>DNA agarose gel electrophoresis results showed the characteristic "ladder" pattern of apoptosis in HPBLs treated with ST, DON and AFG1. Flow cytometric DNA analysis revealed that typical subdiploid peaks of apoptosis in DNA histogram could be seen in all groups treated with the three mycotoxins. Significant time-effect and dose-effect relationships were found between the apoptosis rates and treatment time as well as concentrations of the three mycotoxins.</p><p><b>CONCLUSION</b>ST, DON and AFG1 can induce apoptosis of HPBLs in vitro and may have some negative effects on human immunosystem.</p>
Subject(s)
Humans , Aflatoxins , Pharmacology , Apoptosis , Dose-Response Relationship, Drug , Electrophoresis, Agar Gel , Flow Cytometry , Food Contamination , Lymphocytes , Cell Biology , Sterigmatocystin , Pharmacology , Time Factors , Trichothecenes , PharmacologyABSTRACT
Objective: To explore the inhibitory effect of artesunate(Art)on human esophageal carcinoma cells and to study the related mechanism.Methods: Nude mice were inoculated with Eca109 cells subcutaneously on the left upper limbs to establish esophageal carcinoma model.The model mice were divided into 5 groups: first group received 100 mg/kg Art,second group 200 mg/kg Art,third group 300 mg/kg Art,forth group 3 mg/kg cisplatin(DDP),and the fifth group received normal saline.Mass and volume changes of transplant tumors in different groups were observed.Flow cytometry was used to detect the cell cycle,apoptosis,and the expression of CDC25A protein,Smad3 protein and TGF-?protein in the transplanted tumors in mouse model.RT-PCR was used to detect the expression of CDC25A,Smad3 and TGF-?mRNA in the transplanted tumors.Results: Nude mouse model bearing human esophageal carcinoma was success- fully created.Compared with the control group,the volume and mass of transplant tumors in Art groups were significantly smaller(P
