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Objective To investigate the levels of miR-1 9a and miR-1 9b expressions in cancer tissues and serum of patients with non-small cell lung cancer (NSCLC),and evaluate the potential of miR-1 9a and miR-1 9b as biomarkers of NSCLC.Methods Real time-PCR was used to detect the expressions of miR-1 9a and miR-1 9b in serum of normal people and patients with NSCLC and in cancer tissues and their corresponding non-tumor tissues. The diagnostic value of miR-1 9a and miR-1 9b for NSCLC was assessed by receiver operator characteristic (ROC) curve.Results The expression levels of serum miR-1 9a and miR-1 9b were significantly higher in patients with non-small cell lung cancer than in normal people (P <0.05 ).The expressions of miR-1 9a and miR-1 9b in NSCLC were much higher than in the adjacent normal tissues.For miR-1 9a the area under ROC curve was 0.989,and the sensitivity and specificity were 95.1 and 94.0.The area under ROC curve for miR-1 9b was 0.983,and the sensitivity and specificity were 93.4 and 94.0.Conclusion The high expressions of miR-1 9a and miR-1 9b are found in cancer tissues and serum from NSCLC patients.Therefore,they may be used as noninvasive biomarkers for diagnosis and prognosis of NSCLC.
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Objective To investigate the effect of amiloride on the invasion capacity of esophageal carcinoma EC9706 cell line in vitro and to elucidate its possible mechanism.Methods The invasion capacities of EC9706 cells pretreated with amiloride were measured by transwell chamber assay. The urokinase-type plasminogen activator (uPA) transcription were determined by RT-PCR.The protein expression of uPA were assessed by Western blot.Results After the EC9706 cells were pretreated with amiloride at different concentrations,the number of invaded cells was obviously less than those of control group with obvious dosage dependent pattern (96±7,78±6,57±6,33±4,15±3,F =43.46,P ＜ 0.01).The transcription levels of uPA mRNA and the protein expression levels of uPA in EC9706 cells decreased significantly compared with the control (mRNA:0.623±0.065,0.526±0.054,0.389±0.041,0.312±0.038,0.247±0.025,F =6.71,P ＜0.01; protein:0.732±0.064,0.644±0.057,0.533±0.058,0.391±0.036,0.267±0.043,F =6.71,P ＜0.01).Conclusion Amiloride inhibits the invasion capacity of esophageal carcinoma EC9706 cells.The mechanism might be associated with down-regulation of the expression of uPA.
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Objective To investigate the expression and influence to tumor angiogenesis of urokinase-type plasminogen activator (uPA) and vascular endothelial growth factor (VEGF) in esophageal carcinoma. Methods The expression of uPA and VEGF in the tissue of normal (18 cases) and esophageal carcinoma (68 cases) were evaluated by SP immunohistochemistry, CD34 was detected as marking tumor microvessel density (MVD). uPA and VEGF expression were assessed as to the pathologically biological features of esophageal cancer and to the influence to tumor angiogenesis. Results The positive rates of uPA were 27.8 % (5/18) and 70.6 % (48/68) in the tissue of normal and esophageal carcinoma, respectively, there was significant difference in two tissues (x2 =11.63, P 0.05), but associated with clinical stage, histologic grading and lymph node metastasis (P <0.05). Conclusion Rising expression levels of uPA and VEGF are common in esophageal carcinoma. Altered expression of uPA and VEGF may contribute to tumor angiogenesis of esophageal carcinoma, whose overexpression indicate worse prognosis.
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<p><b>OBJECTIVE</b>To observe the effects of temporary acid exposure on cell proliferation and extracellular signal-regulated protein kinase (ERK) activity in normal human esophageal epithelial cells in vitro.</p><p><b>METHODS</b>Normal human esophageal epithelial cells cultured in vitro were exposed to acidic media (pH 4.0-6.5) for 3 to 60 min, and the control cells were cultured at pH 7.3. MTT assay and flow cytometry were employed for cell proliferation assessment. The expression of phosphorylated ERK1/2 protein was determined by immunoblotting.</p><p><b>RESULTS</b>Esophageal epithelial cells with acid exposure for 3 min exhibited a significant increase in cell proliferation, increased number of cells in S phase and enhanced expression of phosphorylated ERK1/2 protein. Acid exposure of the esophageal epithelial cells exceeding 6 min resulted in depressed proliferation and decreased S-phase cells, and cell proliferation induced by acid exposure was abolished by pretreatment with U0126.</p><p><b>CONCLUSION</b>Temporary acid stimulus increases cell proliferation of normal human esophageal epithelial cells in vitro by activating the ERK pathway.</p>
Subject(s)
Humans , Acids , Pharmacology , Blotting, Western , Butadienes , Pharmacology , Cell Proliferation , Cells, Cultured , Culture Media , Pharmacology , Enzyme Inhibitors , Pharmacology , Epithelial Cells , Cell Biology , Metabolism , Esophagus , Cell Biology , Extracellular Signal-Regulated MAP Kinases , Metabolism , Hydrogen-Ion Concentration , Immunohistochemistry , Keratin-14 , Nitriles , Pharmacology , Signal Transduction , Time FactorsABSTRACT
Objective To study the effect and mechanism of increase in radio sensitivity of kidney cancer cells(GRC-1) induced by ?-elemenen in vitro. Methods GRC-1 cells were divided into 3 groups, blank group (added with 2 mL culture medium), emulsion group (added with 2 mL blank emulsion culture medium) and drug group (added with 2 mL 50 mg?L -1 ?-elemenen culture medium). After been cultivated for 24 hours, the cells were irradiated using 6MeV X-linear accelerator in different doses at the rate of 400cGy per minute. Number of cell clones was counted, and radiation-survival curve of GRC-1 cells was drawn. Flow cytometry (FCM) was used to measure cell cycle and apoptosis. Cells of climbing flake were dyed by immunocytochemical method, the gene expression of bcl-2 and PCNA was measured by imaging system. Results The cell cycle showed that the G 2M blocking caused by 50 mg?L -1 ?-elemenen was enhanced with time increase. It reached peak at 24 hours. FCM showed that the level of apoptosis increased with increase in drug dose and action time. The gene expression of bcl-2 was decreased by 20% in drug group than that in blank group, but there was no expression of PCNA in the two groups. Conclusion The radiosensitivity of GRC-1 cells can be enhanced by ?-elemenen. The mechanism of effect may be associated with the cell cycle blocking, inducing cell apoptosis and down-regulating expression of bcl-2 gene.