ABSTRACT
PURPOSE: To investigate the effect and mechanism of phospholipase C epsilon gene 1 (PLCE1) expression on esophageal cancer cell lines. MATERIALS AND METHODS: The esophageal carcinoma cell lines Eca109 and EC9706 and normal esophageal epithelial cell line HEEC were cultured. The expression of PLCE1, protein kinase C alpha (PKCα), and nuclear factor kappa B (NF-κB) p50/p65 homodimer in cells were comparatively analyzed. The esophageal cancer cells were divided into si-PLCE1, control siRNA (scramble), and mock groups that were transfected with specific siRNA for PLCE1, control siRNA, and blank controls, respectively. Expression of PLCE1, PKCα, p50, and p65 was detected by Western blotting. Transwell assay was used to detect migration and invasion of Eca109 and EC9706 cells. RESULTS: Compared with HEEC, the expression of PLCE1, PKCα, p50, and p65 was increased in Eca109 and EC9706 cells. The expression of PLCE1 was positively correlated with the expression of PKCα and p50 (PKCα: r=0.6328, p=0.032; p50: r=0.6754, p=0.041). PKCα expression had a positive correlation with the expression of p50 and p65 (p50: r=0.9127, p=0.000; p65: r=0.9256, p=0.000). Down-regulation of PLCE1 significantly decreased the expression of PKCα and NF-κB-related proteins (p65: p=0.002, p=0.004; p50: p=0.005, p=0.009) and inhibited the migration and invasion of Eca109 and EC9706 cells. CONCLUSION: PLCE1 activated NF-κB signaling by up-regulating PKCα, which could promote invasion and migration of esophageal cancer cells.
Subject(s)
Blotting, Western , Cell Line , Down-Regulation , Epithelial Cells , Esophageal Neoplasms , NF-kappa B , Protein Kinase C-alpha , RNA, Small Interfering , Type C PhospholipasesABSTRACT
ObjectiveTo study the changes of the plasma thrombomodulin(TM) and von Willebrand factor (vWF) levels and their clinical significance associated with the extent and severity of acute ischemie colitis.MethodsThe plasma TM and vWF levels were determined by enzyme linked immunosorbent assay in 46 patients with acute ischemic colitis (acute ischemic colitis group),42 patients with ulcerative colitis (ulcerative colitis group) and 40 healthy subjects (control group).ResultsThe plasma TM was (49.6 ±2.3) μg/L,and vWF was(198.8 ±8.9)％ in acute ischemic colitis group.The plasma TM was (38.2 ± 3.8) μ g/L,and vWF was ( 162.6 ± 7.6)％ in ulcerative colitis group.The plasma TM was (23.8 ±2.3) μg/L,and vWF was ( 116.7 ± 6.2)％ in control group.The plasma TM and vWF levels in acute ischemic colitis group were higher than those in ulcerative colitis group and control group (P ＜ 0.05 or ＜ 0.01 ).The plasma TM and vWF levels in ulcerative colitis group were higher than those in control group (P＜ 0.05).The plasma TM levels[(49.9 ± 0.3 ) μg/L] and vWF [(210.6 ± 8.2 ) ％] in all colon disease were higher than those in partial colon disease (P ＜ 0.05 ).ConclusionThe changes of plasma TM and vWF levels can be used as one of the indicators for assessment of the development and the prognosis of acute ischemic colitis.
ABSTRACT
ObjectiveTo study changes of molecular markers of prothrombotic state:Platelet granule membrane protein ( GMP-140 ),Von Willebrand factor ( vWF:Ag),thrombomodulin (TM),Two-D dimer ( DD),antithrombin Ⅲ ( AT- Ⅲ ) in plasma and puerarin for treatment functions of acute pancreatitis (AP).MethodsIn 78 patients with AP [ severe acute pancreatitis (SAP):26 cases,mild acute pancreatitis (MAP):52 cases ],using a random number table,the patients were given puerarin treated base (n =40) and conventional treated base group (n =38 ).The two groups were given fast,continuous gastrointestinal decompression,correction of electrolyte and acid-base balance disorders,vein support,antisecretory drugs,antibiotics inhibit pancreatic secretion and inhibition of trypsin activity of drug treatment.Puerarin group:Puerarin injection 0.5 g in 5％glucose injection intravenous infusion of 500 ml,1 time a day.GMP-140 vWF:Ag,TM,DD were measured by the methods of analysis of enzyme-linked immunosorbent assay and AT-Ⅲ was measured by the methods of analysis of chromogenic substrate method preformed in all patients,plasma amylase and uric amylase were determined by the method of somogyi and after the treatment.And 22 healthy people were selected as normal controls ( NC,Group C,n =22).ResultsCompared with the Group C and MAP,the plasma GMP-140 [ ( 86.26 ± 15.28 )ng/Lvs (32.56 ± 18.17) ng/L and (58.68 ± 15.86)ng/L],vWF[(236.22 ±31.78)％vs (95.12 ±31.68)％ and (126.68 ± 17.06)％ ],TM [(65.70 ± 12.27) μg/L vs (4.26 ±0.92) μg/L and (9.80 ± 6.98) μg,/L],DD [ (0.87 ±0.04) mg/L vs (0.36 ±0.06) mg/L and (0.56 ±0.05) mg/L] were significantly elevated,however the AT-Ⅲ [ (56.13 ± 15.78) U/ml vs (98.76 ±22.68) U/ml and (80.38 ± 18.29)U/ml )was significantly decreased SAP ( P ＜ 0.01 ).There were significant differences on the levels of GMP-140 [ (31.52 ± 15.81 ) ng/L vs (59.62 ± 13.73 ) ng/L,t =- 23.283 ],vWF [ ( 93.32 ± 28.62) ％ vs ( 128.81 ±16.23)％,t=-28.205,P＜0.01 ],TM[ (4.36 ± 0.82) μg,/L vs (11.23 ± 7.62)μg/L,t =-43.419,P ＜0.001],DD[ (0.32 ±0.05) mg/L vs (0.68 ±0.04) mg/L,t =- 15.642,P ＜0.001],AT-Ⅲ ((97.68 ±21.69) U/ml vs (76.86 ± 17.92) U/m,t =14.967,P ＜ 0.01 ) between puerarin treated base group and conventional treated base group.Comparing with treated base,the group given puerarin obviously shortened the increased of plasma [ ( 81.26 ± 17.12) U/L vs ( 119.63 ± 51.87 ) U/L,t =- 7.618,P ＜ 0.001 ],uric amylase [ (416.37 ± 116.50) U/L vs (576.32 ± 126.58) U/L,t =- 36.659,P ＜ 0.001 ],the time of abdominal pain relief and therapy to spend [ ( 2.18 ± 0.76 ) d vs ( 5.26 ± 0.58 ) d,t =- 13.619,P ＜ 0.001 ].Conclusion The molecular markers of prothrombotic state:GMP-140,vWF:Ag,TM,DD,AT- Ⅲ might all play key roles in the development of AP.Puerarin can improve the pancreatic microcirculation and adjust molecular markers of prothrombotic state,and had certain treatment functions with AP.