共查询到20条相似文献，搜索用时 46 毫秒
1.
AIM: To investigate relationship between activity of matrix metalloproteinases-2 (MMP-2, 72 kD) and invasion, metastasis of breast cancer. METHODS: Useing zymography and computer software assisted analysis, the activitive levels of MMP-2 (72 kD) in tissues from breast cancer were measeured. RESULTS: Mean activitive levels of MMP-2 72 kD (13.93±3.60) in breast cancer were lower than those in benign disease (21.43±8.31), P<0.05. There was no difference (P>0.05) in MMP-2 62 kD+72 kD of benign and malignant disease, but MMP-2 62 kD (13.83±4.53) and MMP-2 62 kD/62 kD+72 kD(0.48) respectively were significantly higher in malignant disease (P<0.01). It was also found that MMP-2 62 kD/62 kD+72 kD were apparently higher in invasive carcinomas (0.48) and lymph node metastases (0.61), P<0.01, respectively. CONCLUSION: These results demonstrated that a clear relationship between MMP-2 activity and the invasion and metastasis of breast carcinoma. 相似文献
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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
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SU Lian-xiu CHEN Jing-ping YANG Da-ping ZHONG Zai-chan HUANG Li-fang SONG Jian-hua WEI Cui-rong 《园艺学报》2019,35(7):1169-1175
AIM:To evaluate the effect of biological clock gene Timeless (TIM) silencing on the apoptosis and invasion ability of human ovarian cancer SKOV3 cells. METHODS:The protein expression of TIM in the ovarian cancer tissues and normal ovarian tissues was detected by immunohistochemistry, and the correlation between the protein expression of TIM in ovarian cancer tissues and the pathological features was analyzed. The ovarian cancer SKOV3 cells were transfected with PBS (blank control group), control siRNA (siRNA control group) or TIM siRNA (TIM siRNA group). The protein expression of TIM, Bcl-2, Bax, MMP-2, MMP-9, caspase-3 and caspase-9 was determined by Western blot. The apoptosis was detected by flow cytometry. The invasion ability was measured by Transwell chamber test. RESULTS:The positive expression rate of TIM in the ovarian cancer tissues (84.0%) was significantly higher than that in the normal ovarian tissues (10.0%; P<0.01). TIM expression was associated with ovarian cancer differentiation, depth of invasion, lymph node metastasis and TNM stage (P<0.05), but was not associated with age and pathological type (P>0.05). The protein expression levels of TIM, MMP-2, MMP-9 and Bcl-2 in TIM siRNA group were significantly decreased as compared with control group and siRNA control group (P<0.01), and the protein expression of Bax, caspase-3 and caspase-9 in TIM siRNA group was significantly increased as compared with blank control group and siRNA control group (P<0.01). No significant difference of the protein expression of TIM, MMP-2, MMP-9, Bcl-2, Bax, caspase-3 and caspase-9 between blank control group and siRNA control group was observed (P>0.05). The apoptotic rate in TIM siRNA group was significantly higher than that in blank control group and siRNA control group (P<0.01), and that in blank control group and siRNA control group was not significantly different (P>0.05). The penetrated cell number in TIM siRNA group was significantly less than that in blank control group and siRNA control group (P<0.01), and that in blank control group and siRNA control group was not significantly different (P>0.05). CONCLUSION:Silencing of TIM gene in ovarian cancer SKOV3 cells by siRNA promotes apoptosis, and inhibits cell invasion. 相似文献
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AIM:To study the effect of berberine(Ber) on invasion and migration of PG cells from a high metastatic human giant lung carcinoma cell line and to explore its mechanism. METHODS:Agarose drop method was used to detect PG migration; transwell cabin with FN in lower chamber was adopted to detect PG chemotaxis. PG adhesion to FN and martrigel was detected by MTT; PG invasive ability was determined by transwell cabin covered with martrigel. Expression of MMP2/TIMP2 protein and mRNA were detected by quantitative immunocytochemical method and RT-PCR respectively. RESULTS:After PG was treated by Ber（10 mg/L） for 24 h: 1) migration distance of Ber-treated PG cells was markedly shorter than that of control cells (P<0.01) and the number of passed membrane cells towards FN was much fewer than that of control cells (P<0.01); 2) PG adhesion to FN and martrigel was inhibited remarkably by Ber compared with control PG; 3) the migration of PG cells through the martrigel-coated transwell was significantly inhibited by the addition of Ber; 4) MMP2 expression was reduced significantly(P<0.01), while the TIMP2 expression showed up-regulating tendency, but had no differences compared with control group(P>0.05). The MMP2/TIMP2 ratio was decreased; 5) the MMP2 mRNA/TIMP2 mRNA ratio was decreased by Ber.CONCLUSION:Inhibition of cell migration, adhesion to ECM and invasion into ECM of tumor cells and regulation of homeostasis between MMPs and TIMPs to maintain ECM integrity may be the basic mechanism of inhibitive effect of Ber on invasion and metastasis of tumors. 相似文献
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AIM:To study the expression of metastasis suppressor gene KAI1 mRNA in osteosarcoma tissue and osteosarcoma cell lines,and the relationship between it and the biological behavior of the tumor cells.METHODS:RT-PCR was used to detect KAI1 mRNA in 18 cases of resected fresh osteosarcoma samples and three cultured osteosarcoma cell lines.The proliferative rate,the adhesive and invasive abilities of the 3 cell lines were detected.The results were treated by analysis system of images and analyzed with t test.RESULTS:The relative amount of KAI1 mRNA in osteosarcomas with lung metastasis was 0.80±0.50,while that was 1.48±0.64 in osteosarcomas without lung metastasis,the former was significantly lower than the latter (P<0.05).However,KAI1 mRNA had no corelation with the recurrence of osteosarcoma.The expression of KAI1 mRNA in U2-OS was highest (P<0.05),while the proliferation rate,the adhesive and invasive ability of U2-OS were the lowest among the 3 cell lines (P<0.01).CONCLUSION:The metastasis suppressor gene KAI1 might take part in influencing the lung metastasis of osteosarcoma,which might be caused by inhibiting the tumor cell proliferation,adhesion and invasion. 相似文献
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AIM:To observe the expression of long noncoding RNA TTTY15 in osteosarcoma tissues and cell lines and to explore its effect on the viability and invasion ability of osteosarcoma cell lines. METHODS:qPCR was used to detect the expression of TTTY15 in 11 cases of osteosarcoma and its adjacent tissues. The mRNA levels of TTTY15 in osteosarcoma cell lines (143B, Saos2, MG-63, U2OS and HOS) and human osteoblast cell line hFOB1.19 were also tested. TTTY15 was down-regulated after transfected with small interfering RNA in MG-63 cells, the cell line with the highest level of TTTY15. The effect of TTTY15 knockdown on the viability of MG-63 cells was measured by CCK-8 assay. The cell cycle distribution was analyzed by flow cytometry. The effect of TTTY15 knockdown on the cell invasion ability was detected by Transwell assay. The levels of miR-216b-5p and FOXM1 mRNA were detected by qPCR, and the changes of the related proteins were determined by Western blot. RESULTS:Compared with the adjacent tissues, the expression of TTTY15 increased in the osteosarcoma tissues (P<0.01). Compared with the human osteoblast cell line, the expression of TTTY15 increased in the osteosarcoma cell lines (P<0.05), and the level of TTTY15 in the MG-63 cells was the highest (P<0.01). After knockdown of TTTY15 expression in the MG-63 cells, the cell viability was decreased (P<0.05), cell cycle progression was inhibited (P<0.01), and the cell invasion ability was decreased (P<0.01). The expression of miR-216b-5p was increased (P<0.01) and the expression of FOXM1 mRNA was decreased (P<0.01). The protein expression of FOXM1, CDK4, cyclin D1, MMP-2 and N-cadherin was decreased, while the protein expression of E-cadherin was increased (P<0.05). CONCLUSION:The expression of TTTY15 is increased in the osteosarcoma tissues and cell lines. The low expression of TTTY15 inhibits the cell viability and invasion ability of osteosarcoma cells. The possible mechanism is that the knockdown of TTTY15 expression results in the increase in miR-216b-5p expression and the down-regulation of FOXM1 expression. 相似文献
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AIM：To investigate the effects of p21-activated kinase 6 (PAK6) on the invasive and migratory abilities of human non-small-cell lung cancer A549 cells. METHODS：The expression of PAK6 mRNA in A549 cells, human bronchial epithelial (HBE) cells, non-small-cell lung cancer tissues and paired adjacent non-tumor tissues was measured by real-time PCR. After A549 cells were transfected with siRNA-PAK6 (siPAK6) or negative control (NC) for 48 h, the expression of PAK6 at mRNA and protein levels was measured by real-time PCR and Western blotting, respectively. The invasion and migration of A549 cells were detected by Matrigel invasion assay and Transwell migration assay. The cytoskeletal changes were observed with FITC-phalloidin staining under confocal microscope. RESULTS：The level of PAK6 mRNA in A549 cells was higher than that in HBE cells (3.50±1.16 vs 1.12±0.42, P<0.05). The level of PAK6 mRNA in non-small-cell lung cancer tissues was higher than that in paired adjacent non-tumor tissues (5.13±1.33 vs 1.08±0.37, P<0.05). The expression of PAK6 protein decreased by 72% in A549 cells transfected with siPAK6 (P<0.05), and the level of PAK6 mRNA significantly decreased in A549 cells transfected with siPAK6 (3.72±0.75 vs 0.69±0.21, P<0.05). Matrigel invasion assay and Transwell migration assay demonstrated that knockdown of PAK6 markedly attenuated the invasion and migration of A549 cells (P<0.05). The cytoskeletal actin remodeling and reduction of stress fibers in A549 cells transfected with siPAK6 were observed under confocal microscope. CONCLUSION：PAK6 may affect the invasive and migratory abilities of non-small-cell lung cancer cells by cytoskeletal actin remodeling. 相似文献
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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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YANG Ping L&# Shang-rui LI Wen-ling ZHANG Yu-qin PAN Qi XU Meng-yao YANG Bo HU Ya-e 《园艺学报》2019,35(7):1153-1162
AIM:To evaluate the expression and biological role of Toll-like receptor 4 (TLR4) in human non-small-cell lung cancer (NSCLC) cells. METHODS:The mRNA and protein levels of TLR4 in NSCLC tissue were exa-mined by RT-qPCR, Western blot, and immunohistochemistry. After treating the A549 cells and SPC-A-1 cells with TLR4 stimulator lipopolysaccharide (LPS) and inhibitor TAK-242, RT-qPCR, Western blot and flow cytometry were performed to detect the expression of TLR4. The migration and invasion abilities were detected by Transwell assay, and the mRNA expression of matrix metalloproteinase (MMP)-2, MMP-9, and vascular endothelial growth factor (VEGF) was also detected. RESULTS:The mRNA and protein levels of TLR4 were higher in the NSCLC tissue than those in the noncancerous tissue (P<0.01). LPS stimulation significantly increased the mRNA and protein expression levels of TLR4 in the NSCLC cell lines A549 and SPC-A-1 (P<0.01). The LPS-induced TLR4 activation enhanced the migration and invasion abilities of A549 cells and SPC-A-1 cells (P<0.01). LPS increased the expression levels of MMP-2, MMP-9 and VEGF in the A549 cells and SPC-A-1 cells (P<0.01). Moreover, the expression levels of TLR4, MMP-2, MMP-9 and VEGF, as well as the migration and invasion abilities of the cells were blocked by TAK-242 (P<0.01). CONCLUSION:TLR4 might be involved in the migration and invasion of NSCLC cells, and TLR4 inhibition might be considered as a therapeutic target for treatment of NSCLC. 相似文献
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AIM：To investigate the role of benazepril on extracellular signal-regulated kinase (ERK) activity and expression of B-type natriuretic peptide in spontaneously hypertension rat (SHR).METHODS：Wistar Kyoto rats were used as control group.Twenty one 14-week-age SHR were randomized into 3 groups,7 rats each：benazepril group (10 mg·kg-1·d-1);hydralazine group (10 mg·kg-1·d-1) and sham group.In each group drugs or equal volume of vehicle (0.5% carboxymethyl cellulose) were administered respectively for 10 weeks by gavage.The ratio of left ventricle weight to body weight （LVW/BW） was measured to reflect myocardial hypertrophy.The caudal arterial pressure was measured by tail-cuff.Protein expression of p-ERK in myocardial tissue was detected by Western blotting,BNP mRNA in myocardial tissue was examined by RT-PCR,and protein expression of plasma BNP was detected by ELISA.RESULTS：1.Benazepril and hydralazine lowered the blood pressure after 10 weeks treatment (P<0.01).2.The ratio of LVW/BW in SHR benazepril group was significantly lower than that in SHR hydralazine group and SHR sham group (P<0.01),and similar to that in WKY group (P>0.05).3.The protein expression of p-ERK in myocardial tissue in SHR benazepril group was significantly lower than that in SHR hydralazine group and SHR sham group (P<0.01),and similar to that in WKY group (P>0.05).There was no significant difference of p-ERK expression between SHR hydralazine group and SHR sham group (P>0.05).4.The levels of plasma BNP and BNP mRNA in myocardial tissue in SHR benazepril group were significantly lower than that in SHR hydralazine group and SHR sham group (P<0.01),and similar to that in WKY group (P>0.05).There was no significant difference of plasma BNP and BNP mRNA in myocardial tissue between SHR hydralazine group and SHR sham group (P>0.05).CONCLUSIONS：Benazepril inhibited ERK activation,resulting in regression of myocardial hypertrophy and accompanied by the reduction of BNP level.However,in spite of the effect of lowering blood pressure,hydralazine did not prevent or regress cardiac hypertrophy and did not decrease the level of p-ERK and BNP in SHR.BNP level might serve as a therapeutic index for reversal of myocardial hypertrophy. 相似文献
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AIM：To study the influence of Raptor on the invasion ability of glioma cells. METHODS：The technique of RNA interference was used. U87 cells were transfected with Raptor restricted siRNA plasmid, and the expression level of Raptor in the transfected cells was detected by Western blotting. The invasive ability of the cancer cells in vitro was determined. The phosphorylation level of ARK5 and the expression of MMP-2 and MMP-9 were detected by Western blotting. The expression levels of Raptor in the tumor samples of low-grade gliomas (WTO grade I and grade II) and high-grade gliomas (WTO grade III and grade IV) were also analyzed by immunohistochemical staining. RESULTS：Raptor siRNA was transfected into U87 cells and the cells were named siRaptor/U87 cells. The cells transfected with the control plasmid was named Scr/U87 cells. The expression level of Raptor in siRaptor/U87 cells was lower than that in Scr/U87 cells. The results of in vitro invasion assay showed that the number of siRaptor/U87 cells penetrating the Matrivgel matrix membrane was less than that of Scr/U87 cells (P＜0.01). The protein expression of MMP-2 and MMP-9, and phosphorylation of ARK5 protein in the cells in the experimental group were lower than those in control group. The correlation between the expression of Raptor in gliomas and the degree of deterioration was also observed (P＜0.01). CONCLUSION：The expression of Raptor may contribute to the invasion ability of glioma cells by phosphorylation of ARK5 and increase in the levels of MMP-2 and MMP-9. 相似文献
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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
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AIM: To study the expression of matrix metalloproteinase-9(MMP-9), matrix metalloproteinase-2(MMP-2) and the tissue inhibitor of metalloproteinase(TIMP-1) in the lung tissue of the hypercapnia rat.METHODS: Forty Wistar rats were randomly divided into a control group (group A, n=20) and hypercapnia group (group B, n=20). Group B received mix gas exposure (6% CO2, 21% O2, 72% N2) 7 h daily for 4 weeks. The parameters we would examine were as follow: arterial blood gas; the mean pulmonary artery pressure;MMP-2,MMP-9, TIMP-1, and NE activity in lung tissue. Masson pigmentation of elasticity fibre was analyzed by computer image analyzer. Histopathological changes of lung tissue were observed under light microscope. The protein expression of MMP (MMP-2, MMP-9) and TIMP (TIMP-1) in lung tissue were determined by immunocytochemistry.RESULTS: Decompensate respiratory acidosis (pH=7.20±0.04, PaCO2=7.84±0.15) developed in group B. The mean pulmonary artery pressure were similar between groups B and A (P>0.05). Tissue edema in the lung, endothelial cell damage of the small blood vessels, pulmonary micro thrombus formations and increased pulmonary capillary permeability were observed in group B. NE activity increased significantly (P<0.01). However, no significant change of MMP-2, MMP-9, TIMP-1 activity was found in group B and group A (P>0.05). There was significant decrease in the relative content of elasticity fibre in lung tissue in group B compared to group A (P<0.01). The expression of MMP-2 protein in the lung tissue of group B was lower than that in group A (P<0.01), but the expression of both MMP-9 and TIMP-1 proteins in the lung tissue in group B were higher than those in group A (P<0.01).CONCLUSION: Hypercapnia rat model is successfully reproduced by exposure of animals to the mix gas exposure (6% CO2, 21% O2, and 72% N2). The pulmonary artery pressure is not affected by hypercapnia. High concentration of CO2 causes increase of NE activity and decrease in the relative content of elasticity fibre. High concentration of CO2 causes the increase of MMP-2 protein expression and decrease in the MMP-9 and TIMP-1 protein expression. 相似文献
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LIU Qiao-ran ZHANG Zai-yun YU Xiao-ming PAN Xiang-lin WANG Juan-dong LIU Jun-li 《园艺学报》2014,30(8):1497-1513
AIM：To investigate the effect of oridonin on the invasion and migration of human lung cancer NCI-H460 cells. METHODS：NCI-H460 cells were divided into high-dose (HD), middle-dose (MD) and low-dose (LD) oridonin groups (cultured with 40, 20 and 10 μmol/L of oridonin, respectively, as experimental groups), and normal (N) group (treated without oridonin as control). The cell growth was observed. The cell proliferation was detected by MTT assay. Boyden chamber was used to determine the cell invasive capacity. The cell migration was also measured. The levels of MMP-2 and MMP-9 were assayed by Western blotting. RESULTS：The cell counts in the experimental groups were lower than that in N group. The cell proliferation was inhibited as the inhibitory rates were 48.94%, 36.17% and 19.15% for HD group, MD group and LD group, respectively. The numbers of the invasive cells were 26.67±5.16 for HD group, 36.17±5.08 for MD group, and 44.33±5.50 for LD group. The migration rates in the experimental groups were lower than that in N group. The expression of MMP-2 and MMP-9 decreased dependent on the oridonin dose as follows: HD group < MD group < LD group < N group. CONCLUSION：Oridonin inhibits the invasion and migration of NCI-H460 lung cancer cells, and reduces the expression of MMP-2 and MMP-9. 相似文献
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YANG Da-chun MA Shuang-tao YANG Yong-jian LI Xiu-chuan ZHANG Ji-hong TANG Bing LI De 《园艺学报》2010,26(11):2130-2135
AIM:To investigate the effect of peroxisome proliferator-activated receptor δ (PPARδ) activation with dietary GW610742X on the expression of matrix metalloproteinase-9 (MMP-9) and fibronectin (FN) in infarcted and remodeling myocardium. METHODS: Wistar rats were divided into 4 groups: control group, sham group, myocardial infarction (MI) group and MI+GW610742X (GW) group. The left coronary artery was ligated to establish the MI model. PPARδ activator GW610742X (100 mg·kg-1·d-1) was given to the rats in GW group. At the 3rd month of the procedure, the expression of PPARδ, MMP-9 and FN at mRNA and protein levels in the left ventricular free wall(LVFW) of the heart from each group was identified and the distribution of FN was detected by immunofluorescence. RESULTS: After 3 months following the procedure, obvious necrosis and fibrosis in LVFW were observed in MI group. The expression of PPARδ in MI group was higher than that in control, sham and GW groups (P<0.01), and PPARδ expression in GW group was lower than that in control and sham group (P<0.05). In MI and GW groups, the expression of MMP-9 was higher while the expression of FN was lower than those in control and sham group (P<0.05 or P<0.01). In GW group, the expression of MMP-9 was lower (P<0.05) while the expression of FN was higher (P<0.01) than those in MI group. Meanwhile, the expression of MMP-9 and FN in sham group was similar to those in control group (P>0.05). CONCLUSION: MMP-9 is upregulated and FN is downregulated in infarcted myocardium during the remodeling process. Activation of PPARδ inhibits the upregulation of MMP-9 and degradation of FN, thus ameliorating the myocardial remodeling. 相似文献
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AIM: To investigate the expression and clinical significance of PAK4 in the cell lines and tissues of non-small cell lung cancer (NSCLC). METHODS: PAK4 expression in human bronchial epithelial (HBE) cells, NSCLC cell lines, NSCLC tissues and adjacent non-tumor tissues were assessed by immunohistochemistry, real-time PCR and Western blot. Prognostic value of PAK4 expression was evaluated by Kaplan-Meier analysis and Cox regression. RESULTS: PAK4 was over-expressed in the NSCLC cell lines at both mRNA and protein levels compared with HBE cells (P<0.05). PAK4 was over-expressed in the NSCLC tissues at both mRNA and protein levels compared with adjacent non-tumor tissues (P<0.05). PAK4 was over-expressed in the metastatic NSCLC tissues compared with the primary NSCLC tissues (P<0.05). Higher PAK4 staining scores were positively correlated with differentiation, lymph node metastasis, distant metastasis, and clinical stage. Kaplan-Meier analysis and log-rank test showed that overall survival was significantly different between the patients with up-regulated PAK4 and the patients with down-regulated PAK4(P<0.05). PAK4 over-expression was associated with NSCLC progression.CONCLUSION: Increased PAK4 expression was associated with tumor invasion, metastasis and prognosis in the patients with NSCLC. PAK4 is an important prognostic marker and potential therapeutic target in NSCLC. 相似文献
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AIM: The present study was undertaken to investigate the effect of angiotensin II (AngⅡ) on expression of MMP-9 in THP-1 macrophages. METHODS: Macrophages converted from THP-1 monocytes by incubating with PMA (0.1 μmol/L) for 48 h were divided into PMA group; PMA+AngⅡ group (10-7mol/L, 1 h); PMA+AngⅡ+PDTC group (10 μmol/L, 30 min) and PDTC group. Western blotting was used to detect the MMP-9 and phosphorylation of NF-κB p65, and the expression of MMP-9 mRNA in THP-1 macrophages was measured by RT-PCR.RESULTS: Compared to control group, the expression of MMP-9 (1.06±0.11, P<0.05) and phosphorylation of NF-κB p65 (1.02±0.10, P<0.05) in THP-1 macrophages were expressed when treated with AngⅡ (10-7mol/L); and the expression of MMP-9 mRNA were upregulated (1.22±0.08, P<0.05). However, NF-κB inhibitor PDTC reduced the NF-κB p65 (0.99±0.12, P<0.01) and MMP-9 (1.04±0.14, P<0.01) expressions and decreased the expression of MMP-9 mRNA (0.90±0.06,P<0.01). CONCLUSION: NF-κB signaling pathway contributes to the expression of MMP-9 in THP-1 macrophage induced by AngⅡ. 相似文献