共查询到20条相似文献，搜索用时 15 毫秒
1.
HOU Wei-hong YUAN Bao-mei WANG Tian-yun CHAI Yu-rong HOU Gui-qin WANG Jian-min XUE Le-xun 《园艺学报》2004,20(6):998-1002
AIM: To clone and express mouse canstatin (m canstatin) cDNA and provide a basis for the further research on its anti-angiogenic activity and potential application for cancer therapy. METHODS: Total RNA was extracted from mouse liver tissue by Trizol Reagent, and mouse canstatin cDNA was amplified by RT- PCR, then cloned into vector pMD18-T for sequencing. pET30a(+)-m canstatin recombinant plasmid was constructed and expressed in E.coli BL21 with induction of IPTG. RESULTS: Mouse canstatin cDNA is 684 bp coding 227 amino acids. The sequences of both cDNA and amino acid share high homology with human canstatin, with cDNA identity at 89% and amino acids identity at 96% to human canstatin. In the present study, pET30a(+)-m canstatin recombinant plasmid was expressed in E.coli BL21. CONCLUSION: Mouse canstatin cDNA has been cloned for the first time. Constructed pET30a(+)-m canstatin recombinant plasmid is highly expressed in E.coli BL21. 相似文献
2.
Angiogenesis plays a key role in progression of prostate cancer. Antigiogenesis becomes a new treament target for prastate cancer. In this review, we focus on the current knowledge of angiogenesis and tumor angiogenesis inhibitor in prastate cancer. 相似文献
3.
AIM: To investigate the effect of DEC1 gene over-expression on the proliferation and invasion abilities of human esophageal cancer ECA109 cells.METHODS: ECA109 cells were transfected with plasmid pcDNA3.1 (-)/DEC1 (DEC1 group) or pcDNA3.1 (-) (vector group). The mRNA and protein levels of DEC1, cyclin D1 and MMP-9 were evaluated by real-time PCR and Western blot, respectively. The effects of DEC1 over-expression on the proliferation and invasion abilities of the ECA109 cells were evaluated by CCK-8 assay, colony formation assay and Transwell test respectively.RESULTS: The DEC1 expression level in ECA109 cells in DEC1 group was significantly higher than that in vector group (P<0.01), but the levels of MMP9 and cyclin D1 expression were opposite (P<0.01). However, both the proliferation and invasion abilities of ECA109 cells in DEC1 groups decreased significantly as compared with those in vector group (P<0.05).CONCLUSION: The over-expression of DEC1 significantly inhibits the proliferation and invasion of ECA109 cells, which may be involved in the expression of cyclin D1 and MMP9. 相似文献
4.
AIM: Through detecting bone marrow angiogenic mediators and inhibitors in aplastic anemia (AA) patients,the value of angionesis in AA pathogenesis was elucidated.METHODS: The patients were divided into severe AA group (SAA,8 patients),non severe AA group (NSAA,10 patients),and normal control group (7 persons),5 patients were observed before treating (group beginning) and getting improvement (group improving).The angiogenic mediators vascular endothelial growth factor (VEGF) and bFGF were detected by ELISA,angiogenic inhibitors IFN-γ and TSP were detected by ELISA and flow cytometry,respectively.RESULTS: The levels of VEGF were lower in SAA group and NSAA group than those in control group significantly (P<0.05),the levels of IFN-γ and TSP were higher than those in control group (P<0.05),especially in SAA group (P<0.01).Compared with group beginning,the level of VEGF was higher in group improving (P<0.05),the levels of IFN-γ,TSP were lower (P<0.05),there was no obviously difference between group beginning and group improving except IFN-γ.CONCLUSION: The dropping of angiogenic mediators and the rising of angiogenic inhibitors may be one reason of reducing the number of microvessel,which result in deficiency in supporting hemapoietic stem cells by bone marrow microenvironment. 相似文献
5.
AIM To investigate the effects of simvastatin （SIM） on the proliferation of esophageal cancer Eca109 cells through NF-κB p65 pathway. METHODS Esophageal cancer Eca109 cells were cultured in vitro and treated with SIM at different concentrations （2 , 4, 8, 16 and 32 μmol/L）. The proliferation of Eca109 cells was measured by MTT assay and plate colony formation assay. The proliferation-related protein levels of cyclin D1, c-Myc, NF-κB p65 （p65） and IκB-α in the esophageal cancer Eca109 cells were determined by Western blot. ELISA was used to detect the levels of tumor necrosis factor α （TNF-α） and interleukin-6 （IL-6） in the culture supernatant of Eca109 cells. RESULTS Compared with control group, the inhibitory effects of SIM at 2 , 4 , 8 and 16 μmol/L on the viability of Eca109 cells were increased in a concentration-dependent and time-dependent manners （P <0.05）. Simultaneously, the inhibitory rates of SIM at 16 and 32 μmol/L on the viability of Eca109 cells showed no significant difference （P >0.05）. The inhibitory rates of SIM at 16 μmol/L on the viability of esophageal cancer cells was 50.61% at 48 h, which was closed to half of the inhibitory dose IC50, and it was used as the optimum concentration and time for follow-up experiments. Compared with control group, the plate colony formation rate of Eca109 cells, the protein levels of cyclinD1, c-Myc, nuclear p65, TNF-α and IL-6 in 8 and 16 μmol/L groups were decreased, while the levels of cytosolic p65 and IκB-α proteins were increased （P <0.05）. No significant difference of plate colony formation rate in Eca109 cells, and the protein levels of cyclin D1, c-Myc, nuclear and cytoplasmic p65, IκB-α, TNF-α and IL-6 between 16 μmol/L SIM group and 32 μmol/L SIM group was observed （P >0.05）. CONCLUSION Simvastatin inhibits the proliferation of esophageal cancer Eca109 cells, and its mechanism may be related to up-regulation of IκB-α, down-regulation of cyclinD1 and c-myc, inhibition of p65 nuclear translocation, and the expression of TNF-α and IL-6 downstream of NF-κB p65 pathway. 相似文献
6.
The growth and spread of malignant neoplasms largely depend on angiogenesis. Recent studies demonstrate that a various types of neovascularization including angiogenesis, vasculogenesis and vasculogenic mimicry exist in a few highly aggressive tumors. Ovarian carcinoma is the leading cause of death in gynecologic malignancy. Here, we review the effect of angiogenesis, vasculogenesis and vasculogenic mimicry in development and spread of ovarian carcinoma. 相似文献
7.
AIM: To investigate the change of chemosensitivity of esophageal carcinoma cells before and after induction by radiation,and to detect the excision repair cross complementation group 1 (ERCC1) gene before and after induction,and further to analyze the relationship between ERCC1 expression and chemosensitivity.METHODS: The esophageal carcinoma cell EC9706 was radiated repeatedly by a long-term,intermittent ［60Co］-γ radiation to induce the radioresistance esophageal carcinoma cell EC9706-R.The IC50 and resistant index (RI) of EC9706 and EC9706-R were detected by MTT assay.The expression of ERCC1 was examined by immunocytochemistry and RT-PCR.RESULTS: The IC50 of EC9706 and EC9706-R cells to cisplatin were (1.480±0.012) mg/L and (1.836±0.008) mg/L,respectively (P<0.05),and the RI was 1.240±0.015.The tinctorial scores of ERCC1 protein in EC9706 and EC9706-R were 2.838±0.055 and 2.898±0.039 (P>0.05),and the relatively quantities (IDV) of ERCC1 mRNA in EC9706 and EC9706-R cells were 1.168±0.068 and 1.143±0.089 (P>0.05).SP and RT-PCR did not display visible difference in protein level and mRNA level.CONCLUSION: The chemosensitivity of EC9706-R cells to cisplatin is decreased compared with EC9706 cells,but ERCC1 expression does not change with the radioresistance and chemoresistance. 相似文献
8.
QI Cui-ling ZHOU Xin-lei YE Jie YANG Yang ZHANG Qian-qian LI Jiang-chao LAN Tian HE Xiao-dong WANG Li-jing 《园艺学报》2014,30(3):400-403
AIM：To study the effect of andrographolide (Andro) on oral squamous cell carcinogenesis. METHODS：Chemical-induced hamster buccal pouch cancer model was used. The tumor cell proliferation, apoptosis and microvessel density (MVD) were detected by immunohistochemical staining. RESULTS：Compared with control group, the tumor volume, MVD and tumor cell proliferation in Andro group were significantly decreased. The cell apoptotic cell number in Andro group was higher than that in control group. Caspase-3 was also activated in Andro group. CONCLUSION:Andro inhibits tumor growth by suppressing proliferation, decreasing MVD and promoting apoptosis in the hamster buccal pouch. Furthermore, Andro promotes tumor cell apoptosis through caspase-3 pathway. 相似文献
9.
AIM: To investigate the effect of human chorionic gonadotropin(hCG) on cyclooxygenase-2(COX-2) expression in endometrial carcinoma so as to study the function of ectopic hCG.METHODS: The ectopic β-hCG in JEC endometrial carcinoma cell lines was quantified by radioimmunoassay. By MTT assay, the effect of hCG on the cell viability of JEC cell lines and the inhibition of selective COX-2 inhibitor NS398 on JEC cell lines were examined. The effect of hCG on COX-2 expression was detected by Western blotting. RESULTS: The ectopic β-hCG release from cultured JEC cell lines were observed. HCG promoted the cell viability, upregulated the expression of COX-2 protein and increased the inhibition of selective COX-2 inhibitor NS398 in JEC cell lines. CONCLUSION: The ectopic hCG in JEC endometrial carcinoma cell lines increases cell proliferation, which may be mediated by upregulating the expression of COX-2 protein. 相似文献
10.
AIM:To investigate the role of Wnt signaling pathway in the development of radioresistance in esophageal cancer cells. METHODS:The mRNA expression of the genes involved in Wnt signaling pathway was determined by real-time RT-PCR. The protein levels involved in Wnt signaling pathway were also confirmed by Western blotting and immunofluorescence method. Xenograft assay was performed to compare the proliferation ability and tumorigenicity of the cell lines. RESULTS:Up-regulation of Wnt1 induced the activation of Wnt signaling pathway and the variation of the downstream genes. β-catenin was accumulated and nuclear-transferred. The expression of downstream targeted genes such as cyclin D1 and WISP1 was increased. The radioresistant esophageal cancer cells showed higher proliferation ability and tumorigenicity in nude mouse xenograft. CONCLUSION:Wnt signaling-induced acceleration of proliferation is important for the development of radioresistance in esophageal cancer cells. 相似文献
11.
AIM: To investigate the expression and significance of RhoC and Ki-67 in human esophageal squamous cell carcinoma (ESCC) tissues.METHODS: The expression of RhoC and Ki-67 was detected in 52 specimens of ESCC by the method of immunohistochemistry. The clinicopathological features were also analyzed.RESULTS: The expression of RhoC was detected in 32 of the total 52 (61.5%) cases of human ESCC tissues, significantly higher than that in the adjacent histologically normal epithelium, which was only in 11 of 37 cases (29.7%, P<0.05). RhoC expression was closely correlated with clinical tumor-node-metastasis (TNM) stage (P<0.05) and lymph node metastasis (P<0.05) in ESCC. The over-expression of RhoC was positively correlated with Ki-67 in ESCC (r=0.322, P<0.05).CONCLUSION: The over-expression of RhoC protein significantly correlates with advanced TNM stage, lymph node metastasis and cell proliferation ability of ESCC. Therefore, RhoC may be a new auxiliary parameter for early diagnosis and prognostic evaluation of ESCC. 相似文献
12.
AIM: To determine the effect of salvia extract on angiogenesis of the myocardium in the rats with myocardial infarction (MI) and to analyze its possible mechanism. METHODS: Left coronary artery of Sprague-Dawley rats was ligated to establish a MI model. The rats were randomly divided into MI model group, 3 different dose groups of salvia (10, 20 and 40 mg·kg-1·d-1), and sham operation group. Each group consisted of 8 rats. The rats in all treatment groups were orally administered with the salvia extract, and the rats in MI group and sham operation group were fed with the same volume of saline. The rats were sacrificed 4 weeks later. The hemodynamic changes of the rats were determined, and the segmental heart samples were used for morphological observation by hematoxylin and eosin staining, Masson staining, or electron microscopic analysis. The expression of vascular endothelial growth factor (VEGF) and cluster of differentiation 34 (CD34) was analyzed according to immunohistochemistry. RESULTS: Compared with sham operation group, the morphological changes of the myocardium in MI group were disordered, part of myocardial cell outline disappeared, and obvious fibrosis in the necrosis myocardial tissue and fuzzy or disappearing microvascular ultrastructure were also observed. Compared with MI group, the number of new microvessels in all the treatment groups increased obviously, and the morphological changes of the endothelial cells were relatively complete according to electron microscopy. Compared with sham operation group, the protein expression of VEGF and CD34 in the cytoplasm of the myocardial tissues in MI group increased only a little. Compared with MI group, the protein expression of VEGF and CD34 in the cytoplasm of the myocardial tissues in all treatment groups increased significantly (P<0.01). CONCLUSION: Salvia extract obviously promotes angiogenesis of the myocardial tissues in the rats after myocardial infarction. 相似文献
13.
XU Qian ZHAO Ya-ling FU Jian-zhu GU Lei LIU Gui-min LIANG Wen-tong CHENG Zhi-yong 《园艺学报》2015,31(12):2158-2163
AIM: To investigate the effect of AG490 on the expression of VEGF and HIF-1α, and the capacity of invasion in human erythroleukemia (HEL) cells. METHODS: The HEL cells were treated with AG490 at different concentrations. The cell viability was detected by CCK-8 assay. The apoptosis was detected by Hoechst staining. The apoptosis and the cell cycle were analyzed by flow cytometry. The capacity of migration was evaluated by Transwell assay. The mRNA expression level of JAK2 was measured by RT-PCR. The protein levels of p-JAK2, VEGF and HIF-1α were determined by Western blot. RESULTS: The HEL cell viabilities were 88%, 75%, 48%, 10% and 0.12% after treated with AG490 at 20, 40, 60, 80 and 100 μmol/L for 48 h, respectively. The results of Hoechst staining showed that brilliant blue cells in 80 μmol/L AG490 group was significantly increased compared with control group for 48 h. The apoptosis rate of 80 μmol/L AG490 group was significantly increased compared with control group at 48 h after AG490 treatment. The number of membrane-permeating HEL cells in 20 μmol/L AG490 group at 24 h after AG490 treatment was significantly lower than that in control group (P<0.05). The mRNA level of JAK2 decreased in a concentration-dependent manner after the HEL cells were treated with different concentrations of AG490 for 48 h. The protein levels of p-JAK2, VEGF and HIF-1α were lower in AG490 treatment groups than those in control group (P<0.05). CONCLUSION: AG490 inhibits the expression of VEGF and HIF-1α in HEL cells by inhibiting JAK2 pathway. 相似文献
14.
AIM: To explore the effect of N-cadherin knock-down on the biological behavior of EC9706 cells in vivo.METHODS: The control vector pEGFP-MSCVneo and recombinant retroviral vector pMSCVneo/N-cadherin plasmids were transfected into esophageal squamous cell carcinoma(ESCC) cell line EC9706 according to the manufacturer's instructions. Stable EC9706 cell clones were selected using selection medium containing G418. Untreated EC9706 cells, control vector-transfected EC9706 cells and N-cadherin RNAi-transfected EC9706 cells were inoculated subcutaneously into the right flank of BALB/c mice (5 for each group), respectively. When tumors became palpable, the diameters of the tumors were measured with a caliper each week after subcutaneous implantation, and the volume (mm3) and weight (g) of the tumors were also calculated. Immunohistochemistry and Western blotting were employed to examine the expression levels of E-cadherin, N-cadherin and MMP-9 in the tumor tissues. The cell apoptosis was analyzed by TUNEL method.RESULTS: Compared with untreated group and control vector group, there was an obvious decrease in the volumes and weights of the tumors in N-cadherin RNAi group (P<0.05). No difference of E-cadherin expression in the 3 groups was observed. However, the expression of N-cadherin and MMP-9 in N-cadherin RNAi group was apparently reduced, and the positive number of cell apoptosis was obviously increased in N-cadherin RNAi group (106.81±6.47) as compared with that in untreated group (51.55±4.68) and control vector group (54.17±5.26). CONCLUSION: N-cadherin knock-down inhibits the tumor formation of EC9706 cells in nude mice by decreasing MMP-9 expression, resulting in less degradation of ECM and less aggression of the cancer cells. N-cadherin is an important factor in the progression and metastasis of ESCC,and may serve as a potential molecular target for biotherapy of ESCC. 相似文献
15.
AIM: To study the changes and correlations of β-catenin, multidrug resistance-associated protein 2 (MRP2), P-glycoprotein (P-gp), Bcl-2 and the free ATP level in esophageal squamous-cell carcinoma (ESCC) cell line EC-109 induced by ATP-competitive glycogen synthase kinase(GSK-3) inhibitor 6-bromoindirubin-3'-oxime (BIO). METHODS: The methods of flow cytometry, immunofluorescence, cytochemistry and ATP assay were used to study the expression levels of MRP2, P-gp, β-catenin and Bcl-2, the efflux capability of ATP-binding cassette (ABC) transporters, and the free ATP level in ESCC cells. RESULTS: After induced by BIO, up-regulation of β-catenin and Bcl-2 expression in cytoplasm and accumulation of β-catenin in nucleus were found in ESCC cells. The expression of MRP2 was up-regulated in cytoplasm and cell membrane. On the contrary, the expression of P-gp was down-regulated in cytoplasm and cell membrane. The free ATP level and the efflux capability of ABC transporters increased in ESCC cells. CONCLUSION: The multidrug resistance of ESCC cells in enhanced by BIO treatment. 相似文献
16.
AIM: To study the effect of miR-18a on angiogenesis of human aortic artery endothelial cells. METHODS: After 10 nmol/L miR-18a mimics or 20 nmol/L inhibitor was transfected into human aortic endothelial cells, the expression level of miR-18a was determined by qRT-PCR, and the capacities of endothelial cell angiogenesis, such as migration, adhesion and tube formation, were observed. RESULTS: Forty-eight hours after transfection with miR-18a mimics, the expression of miR-18a was as 608 folds as the control (P<0.05), but decreased to 31% of the control level in miR-18a inhibitor transfection group (P<0.05). Compared with control group, the numbers of endothelial cells, which migrated to the lower Transwell chamber and formed capillary-like tubes, declined by 60% and 52%, respectively, in miR-18a mimics group (P<0.01), and they increased by 100% and 84%, respectively, in miR-18a inhibitor transfection group (P<0.05, P<0.01). In addition, the inhibitor treatment group displayed more potent adhesion capacity, 43% higher than that in control group (P<0.05). CONCLUSION: miR-18a is involved in angiogenesis of human arterial endothelial cells, and might be a potential molecular therapeutic target of vascular diseases. 相似文献
17.
ZHANG Wei-guo WU Qing-ming YU Jie-ping WANG Xiao-hu XIE Guo-jian TONG Qiang LIU Chong-zhen 《园艺学报》2004,20(7):1208-1212
AIM: To investigate the effect on growth and activity of telomerase in esophageal carcinoma cells by inhibiting ubiquitin-proteasome pathway(UPP). METHODS: The esophageal carcinoma cell strain Eca9706 was treated with MG-132 to inhibit its UPP specially. The effect of growth suppression on cells was evaluated with MTT assay, morphologic changes of cells were observed under microscope, cell cycle and apoptosis were detected by flow cytometry (FCM). DNA fragment analysis was used to confirm the presence of apoptosis. The activity of telomerase was detected. RESULTS: MG-132 had obvious inhibitory effect on the growth of Eca9706 cells in a dose and time-dependent manner. Obvious pathologic change of cells were observed under microscope, cells became round, small and exfoliating. The FCM analysis showed that the ratio of esophageal carcinoma cells of G1 phase increased and a obviously apoptotic sub-G1 peak was found. Agarose electrophoresis showed marked ladder. The activity of telomerase was obviously inhibited. CONCLUSIONS: MG-132 significantly inhibits the growth and the activity of telomerase of Eca 9706 cells. These findings indicate that inhibiting UPP is a new strategy for the treatment of esophageal carcinoma. 相似文献
18.
TONG Qiang LIU Xiao-bo LUO He-sheng LI Sheng-bao YU Zong-tao ZHANG Ji-cai GAO Bo MENG Jian-chao 《园艺学报》2012,28(12):2278-2282
AIM: To investigate the expression and promoter methylation of tazarotene-induced gene-1 (TIG1) in esophageal squamous-cell carcinoma (ESCC) tissues. METHODS: The methods of methylation-specific PCR and real-time fluorescence quantitative PCR were applied to examine the methylation and mRNA expression of TIG1, respectively, in 43 cases of ESCC tissues, 20 cases of paracancerous tissues and 15 cases of normal tissues. RESULTS: The frequency of promoter methylation of TIG1 gene in ESCC tissues was 25.6% (11/43), which was significantly higher than that in the paracancerous tissues (5.0%, 1/20) and normal tissues (0/20). The hypermethylation of TIG1 gene in these tissues had no correlation with sex, age and clinical stage of the patients. However, it was correlated with the pathological stage (P<0.01) and lymph node metastasis (P<0.05). The mRNA expression of TIG1 in ESCC tissues was significantly lower than that in paracancerous tissues (P<0.05) and normal tissues (P<0.01). However, the expression level of TIG1 mRNA in methylated tissues was significantly lower than that in unmethylated tissues (P<0.01). CONCLUSION: Promoter methylation may be an important mechanism of TIG1 gene inactivation in ESCC, which was related to lymph node metastasis and TNM stage of esophageal carcinoma. 相似文献
19.
AIM: To investigate the promoter methylation of secreted frizzled-related protein(SFRP) genes in esophageal squamous cell cancer(ESCC). METHODS: The methods of methylation-specific PCR(MS-PCR) and RT-PCR were applied to examine the CpG methylation of the SFRP promoter and the mRNA expression of SFRP genes,respectively, in 78 samples of ESCC and corresponding adjacent non-cancer tissues. The protein expression of β-catenin was determined by immunohistochemistry.RESULTS: In the ESCC tissues, the frequencies of promoter methylation in SFRP1 , SFRP2 , SFRP4 and SFRP5 genes were 65.4%(51/78), 69.2%(54/78), 62.8%(49/78) and 52.6%(41/78),respectively, significantly higher than those in the adjacent tissues(P<0.01). The hypermethylation of these genes had no correlation with clinical stage and pathological classification in ESCC tissues(P>0.05). The frequency of simultaneous methylation of the 4 genes was correlated with the clinical stage(P<0.05). The positive rates of mRNA expression of the 4 genes in ESCC tissues were 42.3%(33/78), 46.2%(36/78), 50.0%(39/78) and 39.7%(31/78), respectively lower than those in the adjacent tissues(P<0.01). The mRNA expression of SFRP genes and the ectopic expression of β-catenin were correlated with the methylation frequency of SFRP genes(P<0.01).CONCLUSION: Promoter methylation of SFRP1 , SFRP2 , SFRP4 and SFRP5 genes was a frequent event in ESCC, indicating a contribution to the pathogenesis of ESCC through aberrant canonical Wnt/β-catenin signaling pathway. Combination analysis of methylation status in SFRP genes may has definite value on estimating prognosis of ESCC. 相似文献
20.
LIN Jun SUN Jie ZHOU Yan HUANG Xing XIONG Ping WANG Ya-ping DENG Chang-sheng 《园艺学报》2002,18(9):1112-114
AIM: To probe into the genetic susceptibility of HLA-DRB1 alleles to esophageal neoplasm in Hubei Han Chinese. METHODS: HLA-DRB1 gene polymorphism in 42 patients with esophageal neoplasm and 136 normal control subjects was studied by PCR and sequence. RESULTS: Allele frequency of HLA-DRB1 *0901 allele was significantly higher in esophageal cancer patients than those in normal controls(0.2500 vs 0.1397, P =0.028; the odds ratiO2.053; etiologic fraction 0.1282).There were no association between the rested HLA-DRB1 alleles with patients. CONCLUSION: Individuals carrying HLA-DRB1 *0901 may be susceptible to esophagealo carcinoma, its nucleotide sepuence approachs to the corresponded allele sequence(exoN2)published in GenBank. 相似文献