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1.
AIM:To detect tissue factor (TF) level both in plasma and in tissue of hepatocellular carcinoma (HCC) patients and to elucidate their association with clinical features.METHODS:Plasma TF levels of 50 cases of HCC patients and 30 cases of control were detected by ELISA.27 HCC tissue samples with their adjacent tissue samples and 27 normal liver tissues were detected by RT-PCR.RESULTS:① Plasma TF levels were increased significantly in HCC group when compared with control (P<0.05).TF levels were higher in poor differentiation,large size and cirrhosis subgroup in HCC patients (P<0.05).Plasma TF levels were also significantly increased in extra-hepatic metastasis,lymphatic metastasis and portal venous tumor thrombus subgroups (P<0.05).② The mRNA expression rate of TF in HCC tissue was 62.96% (17/27) and the relative mRNA expression intensity of TF was 0.567±0.268.Those were significantly higher than that in their adjacent tissue samples or 27 normal liver tissue samples (P<0.05).While the relative expressive intension of TF were also significantly higher in larger size and several invasive and metastatic subgroups (P<0.05).CONCLUSION:TF might play an important role in hepatic carcinogenesis,invasiveness and metastasis.  相似文献   

2.
AIM: To investigate the roles of hepatocytes, hepatic stellate cells (HSCs), Kupffer cells (KCs) and endothelial cells (ECs) in the regulation of PA-plasmin system during liver fibrogenesis in rats. METHODS: Experimental liver fibrosis was induced in rats by injection of carbon tetrachloride (CCl4) twice a week for 12 weeks. Four kinds of liver cells were separated from the normal and fibrotic livers of the rats. The expression levels of urokinase plasminogen activator (uPA), uPA receptor (uPAR) and PA inhibitor-1 (PAI-1) in liver cells were determined by Northern and Western blotting. RESULTS: The expression of PAI-1 and uPAR was markedly increased in HSCs during liver fibrosis in rats as compared to those in the ECs. CONCLUSION: HSCs and ECs may play very important roles in the regulation of PA-plasmin system during liver fibrogenesis in rats. The activated HSCs are main cells to secrete PAI-1 and uPAR.  相似文献   

3.
AIM: To study effects of urokinase-type plasminogen activator (uPA) signal transduction on expression of matrix metalloproteinase-2 (MMP-2) and tissue inhibitor of matrix metalloproteinase-3 (TIMP-3) in giant cell tumor of bone (GCT). METHODS: Expression of uPAR, MMP-2 and TIMP-3 in GCT tissue was detected by immunohistochemistry. Phosphorylation level of mitogen-activated protein kinase (p44) in uPA/uPAR signal pathway in cultured GCT cells was detected by immunoprecipitation. The expression of MMP-2 and TIMP-3 in cultured cells after treatment with uPA-ATF or anti-uPAR antibody was also detected by Western blotting. RESULTS: 1) Urokinase-type plasminogen activator receptor (uPAR) was positive on the cell membrane and in cytoplasm of some mononuclear stromal cells (MSCs) and multinucleated giant cells (MGCs); 2) MMP-2 was positive in the cytoplasm and on the cell membrane of almost all of MSCs and some of MGCs. The polar distribution of MMP-2 in the cytoplasm of MGCs was especially obvious; 3) The expression of TIMP-3 of some MSCs and MGCs in GCT was much lower than MMP-2. The positive signal also showed a prominent polarity; 4) After treatment with uPA-ATF, the phosphorylation level of p44 in GCT cultured cells was much higher than the control. Addition of anti-uPAR antibody in the cells remarkably down-regulated the phosphorylation level of p44 as compared with the control group, suggesting that uPA-ATF participates cell signal transduction and this reaction can be inhibited by anti-uPAR antibody; 5) uPA-ATF cell signal pathway up-regulated expression of MMP-2 and TIMP-3, while anti-uPAR antibody down-regulated the expression of MMP-2 and TIMP-3. CONCLUSION: These results demonstrate for the first time that uPA-ATF directly regulates the expression of MMP-2 and TIMP-3 by signal transduction pathway, and the over-expression of MMP-2 and TIMP-3 may play an important role in local osteolysis of GCT.  相似文献   

4.
AIM: To study the effect of ginsenosides on lipopolysaccharide-induced expression of tissue factor (TF) and plasminogen activator inhibitor type-1 (PAI-1) in vascular endothelial cells (EC), and to investigate the mechanism of ginsenosides in the healthy protection and treatment of cardiovascular diseases. METHODS: Human umbilical vein endothelial cells (HUVEC) were cultured by trypsin digestion method. PAI-1 was measured in the conditioned medium of HUVEC by a specific enzyme-linked immunosorbent assay (ELISA), whereas TF activity was measured in the lysates of these cells by a single step clotting assay. Specific mRNA expressions were determined by Northern blotting. RESULTS: Treatment of HUVEC with LPS resulted in a significant increase in PAI-1 antigen and TF activity. Ginsenosides inhibited this LPS-induced upregulation of PAI-1 protein and TF activity in HUVEC. These effects were also confirmed on the level of specific PAI-1 and TF mRNA expression by Northern blotting. CONCLUSION: Ginsenosides counteract endothelial cell activation by inhibition LPS-induced PAI-1 and TF expression in these cells. This ability of ginsenosides might explain its efficacy in the healthy protection and the treatment of cardiovascular diseases.  相似文献   

5.
AIM: To investigate the influence of advanced glycosylation end products-modified bovine serum albumin (AGE-BSA) on mammalian target of rapamycin complex 1 (mTORC1), urokinase-type plasminogen activator receptor (uPAR), and cell mobility in the podocytes, and to further explore the probable relationship. METHODS: The conditionally immortalized mouse podocyte cell line was cultured in vitro. MTT assay and immunofluorescence were used to analyze the cell viability and cytoskeleton of the podocytes treated with the stimuli and intervention agents. The activity of mTORC1 and the expression level of uPAR in normal podocytes and podocytes treated with control BSA or AGE-BSA were detected by Western blotting. The migration ability of the podocytes was determined by would-healing assay. Rapamycin was added to inhibit the activity of mTORC1 along with the addition of AGE-BSA to observe the changes of uPAR and the motility of podocytes. RESULTS: No significant difference of the cell viability or cytoskeleton in the podocytes treated with the stimuli and intervention agents was observed. AGE-BSA up-regulated the activity of mTORC1 and the expression of uPAR, and induced the high mobility of the podocytes. Rapamycin obviously reduced the high expression level of uPAR and the increase in the migration ability of podocytes caused by AGE-BSA treatment. CONCLUSION: AGE-BSA might cause the high migration of podocytes through the mTORC1/uPAR signaling pathway.  相似文献   

6.
AIM: To investigate the function of matrix metalloproteinase-3 (MMP-3) and urokinase-type plasminogen activator receptor (uPAR) to macroangiopathy in type 2 diabetes mellitus. METHODS: The levels of MMP-3 and uPAR in plasma were determined by ELISA sandwich method in 26 healthy controls and 39 patients with type 2 diabetes mellitus including 15 complication-free cases and 24 with macroangiopathy. RESULTS: The plasma level of uPAR but not MMP-3 was higher in patients without macroangiopathy than that in normal controls (P<0.05). In patients with macroangiopathy, the plasma levels of MMP-3 and uPAR were higher than those in normal controls (P<0.01) and patients without angiopathy. There was positive relationship between MMP-3 and uPAR in type 2 diabetes mellitus (r=0.405, P<0.05), and LDL-C was the important affecting factor of uPAR. CONCLUSION: MMP-3 and uPAR are associated with the development of macroangiopathy in type 2 diabetes mellitus. MMP-3 can be regarded as the circulatory markers in type 2 diabetes mellitus with macroangiopathy.  相似文献   

7.
AIM: To observe the effects of Egr-1 gene knockout on the expression of inflammatory-related factors in pancreatic tissue in a mouse acute pancreatitis model. METHODS: The experimental pancreatitis was induced by high-dose of cearulein in wildtype mice and Egr-1 knockout mice. The pancreatitis indexes, such as serum amylase, pancreata edema, and myeloperoxidase(MPO) levels in pancreata and lungs were recorded. The mRNA levels of tissue factor(TF), plasminogen activator inhibitor(PAI-1), monocyte chemoattractant protein(MCP-1), Gro-1, IL-6 and ICAM-1 were measured by quantitative PCR. RESULTS: Contrary to wildtype mice, typical pancreatitis was not induced by high-dose cearulein in the Egr-1 knockout mice, not only markedly reduced edema in pancreata and lungs, but decreased MPO levels in lungs as well were found. Furthermore, the mRNA of TF, PAI, MCAP, ICAM-1 and IL-6 in pancreata were significantly decreased in Egr-1 knockout mice. CONCLUSION: The severity of pancreatitis and lung damage is ameliorated in Egr-1 knockout mice stimulated by high-dosage of cearulein, which was probably mediated by decreasing expression of inflammatory-related factors in pancreata, such as TF, PAI, MCP-1, ICAM-1 and IL-6.  相似文献   

8.
AIM：To study the expression and distribution of somatostatin receptor 2 (SSTR2) during carcinogenesis of hepatocellular carcinoma (HCC) and to evaluate the role of SSTR2 in the carcinogenesis of HCC.METHODS：Experimental HCC model was induced in SD rats using EDNA.SSTR2 mRNA and protein expression were detected by RT-PCR and immunohistochemistry.SSTR2 expression in different tissues at different periods of carcinogenesis were compared.RESULTS：HCC nodule developed after 8 weeks of administration of EDNA.Semi-quantitative analysis showed that SSTR2-mRNA expression in cirrhotic liver tissue at 8 weeks of induction was significantly higher than that in normal liver tissue (1.794±0.212 vs 0.950±0.138,P<0.05).As induction prolonged,SSTR2-mRNA expression increased,and reached its peak level of 2.053±0.169.Then,it decreased gradually.At 22 weeks,SSTR2-mRNA expression decreased to 1.468±0.107,which was significantly lower than the values at 8 weeks and 16 weeks (P<0.05).SSTR2-mRNA in HCC tissue was at low expression level with an average of 1.219±0.249.SSTR2 protein expression was mainly at cytosol and membrane.The change of SSTR2 protein expression in different tissue was consistent with the change of mRNA expression.CONCLUSION：SSTR2 expression was increased at early stage of cirrhosis.At the late stage of cirrhosis and occurrence of HCC,SSTR2 expression was significantly decreased.Down-regulation of SSTR2 may contribute to the carcinogenesis and progression of HCC.  相似文献   

9.
AIM: To investigate the expression of TLR2 and TLR4 in hepatocellular carcinoma (HCC), and to analyze their correlations to clinicopathologic features of HCC. METHODS: The protein and mRNA levels of TLR2 and TLR4 in HCC and para-tumor tissue were determined by immunohistochemistry and real-time fluorescence quantitative PCR (RFQ-PCR). RESULTS: The protein and mRNA levels of TLR2 and TLR4 in HCC were lower than those in para-tumor tissue (P<0.01). At protein level, the intensities of TLR2 and TLR4 expression in HCC and para-tumor tissue were significantly higher than those in normal liver tissue (P<0.01 and P<0.05). Furthermore, the expressions of TLR2 and TLR4 in HCC with cancer embolism in portal vein were weaker than those in HCC without cancer embolism (2= 9.458,P<0.05). CONCLUSION: The intensities of TLR2 and TLR4 expression are lower in HCC than those in para-tumor tissue, whereas higher than those in normal liver tissue. TLR2 and TLR4 signals might take part in the course of HCC.  相似文献   

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11.
AIM:To study the relation between expression of uPAR and annexinⅡ and fibrinolytic activity in various leukemic cell lines. METHODS:The plasma activity was measured under the reaction between cells of NB4, SHI-1, K562, Jurkat, Raji and plaminogen by chromogenic assay. The protein expressions of uPAR and annexinⅡin cells of NB4, SHI-1, K562, Jurkat, Raji were detected by flow cytometry method. The mRNA expressions of uPAR and annexinⅡin cells of NB4, SHI-1, K562, Jurkat, Raji were detected by RT-PCR. RESULTS:The plasma activity in SHI-1 cells and NB4 cells were higher obviously than that in Raji, K562 and Jurkat cells. The protein expression ratio of uPAR and annexinⅡ in NB4 cells were (13.15±1.61)% and (95.97±1.19)%， respectively, they were (99.00±0.26)%, (90.35±2.15)% respectively in SHI-1 cells, and they were lower in K562, Jurkat, Raji cells. The expression of annexinⅡ mRNA in NB4 cells was higher than that in SHI-1 cells, and they were undectectable in K562 and Jurkat cells. The expression of uPAR mRNA in NB4 and SHI-1 cells were higher than that in Jurkat and K562 cells. The expression of uPAR mRNA in Raji cells was undectectable. CONCLUSION:The primary hyperfibrinolysis in leucocythemia cells was observed, and relation was closely with the expression of annexinⅡ. It might be the main reason for bleeding and disseminated intravascular coagulation in patients with acute promyelocytic leukemia and acute monocytic leukemia.  相似文献   

12.
AIM： To study the expression of Smad3 and its significance in hepatocellular carcinoma (HCC) in different species including human, rat and tree shrew, and to verify the feasibility of cross-species oncogenomic approach. METHODS：Real-time fluorescent quantitative polymerase chain reaction and Western blotting were applied to detect the expression of Smad3 at mRNA and protein levels in HCC tissues, corresponding HCC adjacent liver tissues and normal liver tissues collected from different species including human, rat and tree shrew. RESULTS：The mRNA expression of Smad3 in HCC tissues of human, rat and tree shrew was lower than those in the corresponding HCC tissues adjacent liver tissues. The mRNA level of Smad3 in HCC tissues of rat was lower than those in its normal liver tissues, while that in HCC adjacent tissues of tree shrew appeared higher than those in the normal liver tissues. No significant difference of Smad3 expression in other tissues was observed. The protein levels of Smad3 in HCC of human and rat were lower than those in the corresponding HCC adjacent liver tissues and the normal liver tissues. However, the protein expression of Smad3 was at a low level in HCC tissues of tree shrew and was lower than that in the HCC adjacent liver tissues and the normal liver tissues, although without statistical difference. The differences of Smad3 expression between HCC adjacent liver tissues and normal liver tissues in all the 3 species were not statistically significant. CONCLUSION：Smad3 is lowly expressed in HCC tissues of different species, suggesting that it might play a pivotal role in hepatocarcinogenesis and be applied as a key molecular target in HCC prevention and treatment.  相似文献   

13.
AIM: To detect the levels of tissue inhibitor of metalloproteinase-3 (TIMP-3) in both plasma and the tissue of hepatocellular carcinoma (HCC), and to elucidate their association with clinical features.METHODS: Plasma protein levels of TIMP-3 in 56 HCC patients and 30 cases of controls were detected by ELISA.The mRNA and protein levels of TIMP-3 in 30 HCC tissue samples with their portal vein tumor embolus and lymphatic metastasis tissues, and in normal liver tissues from 30 controls were detected by RT-PCR and Western blotting.The relationship between mRNA and protein levels and their clinic-pathological data were analyzed.RESULTS: The plasma TIMP-3 protein levels in the extrahepatic metastasis patients were obviously lower than those in the non-extrahepatic metastasis patients (P<0.05).The mRNA levels of TIMP-3 in normal liver, carcinoma in situ, portal vein tumor embolus and lymphatic metastasis tissues were 0.78±0.09, 0.52±0.09, 0.42±0.07 and 0.40±0.08, respectively, with significant differences among them (P<0.05).The protein levels of TIMP-3 in these 4 kinds of tissues were 115.08±8.60, 77.04±8.83, 64.43±3.80 and 62.80±3.73, respectively, also with significant differences among them (P<0.05).CONCLUSION: The expression of TIMP-3 significantly decreases in the carcinoma in situ tissues of HCC patients, and decreases more obviously in the portal vein tumor embolus and lymphatic metastasis tissues, indicating that low expression of TIMP-3 may play an important role in HCC invasiveness and metastasis.  相似文献   

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17.
ATM: To investigate the effect of tripartite motif-containing protein 44 (TRIM44) on the proliferation of hepatocellular carcinoma (HCC) cells and to study the molecular mechanism. METHODS: The expression of TRIM44 at mRNA and protein levels in normal liver tissues, HCC tissues, adjacent nontumor liver tissues, immortalized hepatocytes and hepatoma cell lines was determined by RT-qPCR and Western blot, respectively. The silencing of TRIM44 was conducted by transfection of vector expressing shRNA targeting TRIM44 (shTRIM44) in the HCC cells, and the protein level of TRIM44 was measured by Western blot. The viability of the HCC cells was analyzed by MTS assay. The DNA synthesis of HCC cells was detected by Click-iT EdU Imaging Kit. The ability of anchorage-independent growth was determined by the method of colony formation on the soft agar. The effects of TRIM44 on the total protein and phosphorylation of mammalian target of rapamycin (mTOR) levels were measured by Western blot. The HCC cells were transfected with shTRIM44 and treated with mTOR agonist MHY1485, and the cell viability was analyzed by MTS assay. RESULTS: The mRNA and protein levels of TRIM44 in the HCC tissues were significantly higher than those in the adjacent nontumor liver tissues and normal liver tissues. In addition, the mRNA and protein levels of TRIM44 in the hepatoma cell lines were significantly higher than those in the immortalized hepatocytes. TRIM44 silencing significantly inhibited the viability of HCC cells and reduced the abilities of DNA synthesis and anchorage-independent growth of the HCC cells. TRIM44 silencing decreased the phosphorylation level of mTOR protein. MHY1485 significantly antagonized the inhibitory effect of TRIM44 silence to the viability of HCC cells. CONCLUSION: TRIM44 silencing inhibits the proliferation of HCC cells possibly through down-regulating the activity of mTOR.  相似文献   

18.
AIM: To investigate the effect of the N-terminal 24-amino acid(N24) overexpression in p55γ re-gulatory subunit of phosphatidylinositiol 3-kinase(PI3K) on the cell adhesion of human gastric carcinoma cell MGC803.METHODS: MGC803 cells, which stably expressed GFP-N24 fusion protein and GFP alone, were generated by transfection with pEGFPN-24 plasmid and control plasmid pEGFP-C1, respectively. The morphological change of the cells was observed under inverted microscope. The expression of GFP-N24 fusion protein was detected by Western blot. The adhesion of the cells was determined by cell adhesion assay. The effects of GFP-N24 fusion protein on the expression of E-cadherin and β-catenin were analyzed by Western blot. The expression and secretion of matrix metalloproteinase 9(MMP9) and urokinase-type plasminogen activator(uPA) in the MGC803 cells were detected by gelatin zymography.RESULTS: MGC803/GFP-N24 cell line steadily expressed GFP-N24 fusion protein and MGC803/GFP cell line steadily expressing GFP were successfully established, but the expression of fusion protein GFP-N24 was lower than that of the control protein GFP. The morphological changes of the transfected cells from paving stone to fibroblast cell form after gene transfection, and the cytoplasm secretory granules were increased significantly. The cell adhesion to fibronectin and collagen decreased after GFP-N24 transfection. GFP-N24 fusion protein increased the expression of cell adhesion molecule E-cadherin and decreased the wnt signal pathway molecule β-catenin in the MGC803 cells. However, it did not affect the expression and secretion of tumor metastasis-related proteins MMP9 and uPA.CONCLUSION: Overexpression of N24p55γ inhibits cell adhesion by influencing the expression of E-cadherin and β-catenin in the MGC803 cells.  相似文献   

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20.
AIM: To study the expression of glypican-3 in hepatocellular carcinoma (HCC) tissues and to clarify its clinical significance. METHODS: The expression of GPC3 was detected in 59 cases of HCC and their para-cancerous tissues, 10 cases of intrahepatic cholangiocellular carcinoma (ICC), 11 cases of cirrhotic tissues and 14 cases of normal liver tissues (around haemangioma) by RT-PCR and immunohistochemical staining. The survival curves were constructed using Kaplan-Meier method and evaluated using the log-rank test. In addition, the Cox proportional hazards regression model was established to identify the factors that were independently associated with disease-free survival (DFS). RESULTS: The mRNA expression of GPC3 in the HCC tissues was significantly higher than that in the para-cancerous tissues (83.1% vs 35.6%, χ2=27.53, P<0.01). The protein expression of GPC3 in the HCC tissue was also higher than that in the para-cancerous tissues (78.0% vs 33.2%, χ2=24.97, P<0.01). The expression of GPC3 in ICC tissues, liver cirrhosis tissues and normal liver tissues was undetectable. Kaplan-Meier survival analysis indicated that the GPC3(+)HCC patients had worse 1-year DFS than that of GPC3(-) patients (33.6% vs 72.7%, P<0.05). The HCC patients with para-cancerous GPC3(+) also had worse 1-year DFS than that of the para-cancerous GPC3(-) patients (23.5% vs 40.1%, P<0.05). The DFS rate decreased significantly as the expression intensity of GPC3 increased. The Cox regression model analysis indicated that AFP(+) (odd ratio=0.372, 95% confidence interval: 0.140-0.900, P<0.05), tumor size (odd ratio=5.215, 95% confidence interval: 1.737-15.656, P<0.01), para-cancerous tissue GPC3(+) (odd ratio=0.226, 95% confidence interval: 0.085-0.599, P<0.01) and the intensity of GPC3 expression in HCC tissue (odd ratio=1.946, 95% confidence interval: 1.080-3.507, P<0.05) were the independent risk factors linked to DFS of patients. CONCLUSION: GPC3 protein is highly expressed in the HCC tissues,but not in ICC, cirrhotic liver and normal liver tissues. The expression of GPC3 in para-cancerous tissues and the intensity of GPC3 expression in HCC tissues are the important independent risk factors linked to DFS of patients.  相似文献   

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