Objective:To systematic review the relationships between the expression of osteopontin (OPN) and esophageal squamous cell carcinoma and its clinicopathologic feature with meta-analyses.Methods: The published studies in the PubMed, the Cochrane Library, EMbase, CBM, CNKI, VIP and WanFang databases were searched, at the time, the documents retrospective method was adopted, and then a series researches about the relationships between the expression of OPN and esophageal squamous cell carcinoma and its clinicopathologic feature were collected. The Jan., 2017 was the deadline of search. The study arranged two researcher to screen documents as the standards of inclusion and exclusion, and extract data and evaluate the quality of methodology for these included documents. The RevMan 5.2 was applied to analyze these data in this Meta analysis.Results: A total of 12 case control studies were included, which included 782 cases of esophageal squamous cell carcinoma in case group and 700 persons in control group. The results of Meta analysis showed the OR of the expression of OPN between cases group and control group was 52.71, and its 95% confidence interval (CI) was 17.95-154.79. Besides, the OR of the expression of OPN between clinical Ⅰ-Ⅱ stage group and clinical Ⅲ-Ⅳ stage group was 0.20, and its 95% (CI) was 0.07-0.60. The OR of the expression of OPN between group with lymph node metastasis and group without lymph node metastasis was 6.37, and its CI was 3.64-11.15. The OR of the expression of OPN between T1+T2 group and T3+T4 group was 0.31, and its 95% (CI) was 0.15-0.64. The differences of the expression of OPN among various group had statistically significant.Conclusion:Current evidence indicates that the expression level of OPN is significantly correlated with esophageal squamous cell carcinoma and its clinicopathologic features. Due to the limited quantity of documents and quality of included studies, above conclusions need to be verified by conducting more high quality studies.

OBJECTIVETo determine the role of zinc finger protein 1 (ZEB 1) in liver fibrosis and in regards to expression of the tumor growth factor-beta (TGFb) signaling factor using a rat model system.

METHODSSprague-Dawley rats were randomly divided into a normal (control) group, liver fibrosis (model) group and a liver fibrosis + therapy (ZEB1 intervention) group. The model group and the ZEB1 intervention group were given intraperitoneal injections of dimethylnitrosamine (DMN) for the first 3 days of each week over a 7-week period; starting at week 5, the ZEB 1 intervention group was started on a routine of every other day tail vein injections of recombinant ZEB1. During this 7-week period, the control group was given intraperitoneal injections of 0.9% NaC1 alone on the DMN schedule. Liver tissues were collected for pathological examination (with hematoxylin-eosin and Masson staining) and for detection of TGFb1 and ZEB 1 expression (by RT-PCR and western blotting). Measurement data were compared between groups using the single-factor analysis of variance test, followed by the least significant difference LSD test. Count data were analyzed by Fisher's exact test.

RESULTSThe model group's liver tissues showed degeneration and necrosis, as well as obvious fibrous septa accompanied by pseudo lobules. The ZEB 1 intervention group's liver tissues showed a significantly higher degree of fibrosis (x²=21.63, P=0), with more coarse fiber cords. The expression of ZEB1 and TGFb1 was significantly higher in the model group than in the control group (both P less than 0.05). However, the ZEB 1 intervention group showed the highest levels of ZEB 1 and TGFb1 expression (vs. model group, P less than 0.05).

CONCLUSIONZEB 1 may promote the development of liver fibrosis in rats through a mechanism involving the TGFb/Smad signaling pathway.

Animals ; Homeodomain Proteins ; pharmacology ; Liver ; drug effects ; metabolism ; Liver Cirrhosis, Experimental ; metabolism ; Male ; Rats ; Rats, Sprague-Dawley ; Transcription Factors ; pharmacology ; Transforming Growth Factor beta1 ; metabolism ; Zinc Fingers

Objective To observe the effect of anti NRP-1 b1/b2 monoclonal antibody (NRP-1mAb) on migration and invasion of gastric cancer cell line BGC-823, and to explore the possible mechanism. Methods NRP-1mAb was prepared in the laboratory, and the purity of antibody was detected by flow cytometry. The different concentrations of NRP-1mAb were added into the culture medium of gastric cancer cell line BGC-823. The migration and invasion of cells after 12 hours was observed by using Transwell method. The phosphorylation of related signal proteins after NRP-1mAb was detected by Western blot analysis. Results When NRP-1mAb prepared by patented technology had the effects on BGC-823 cells after 12 hours, the number of migration and invasion of BGC-823 cells was reduced. The number of cells through the basement membrane in the control group (blank) and the administration group (NRP-1mAb 25, 100, 400 μg / ml) were 167 ± 9, 138 ± 5, 98 ± 5, 36 ± 4, respectively (F = 22.6, P< 0.01); the number of cells through the filtration membrane were 231 ± 40,224 ± 19,176 ± 26,124 ± 34,respectively(F=26.63,P<0.01). There were statistically significant differences between the administered group and the control group at 100 and 400 μg/ml (all P< 0.001). High concentration of NRP-1mAb (100 μg/ml) decreased the phosphorylation level of Akt after 10 minutes' function on gastric cancer cells. However, it was difficult to detect phosphorylated Akt after 30 minutes. Conclusion NRP-1mAb may inhibit the migration and invasion of gastric cancer cell line BGC-823 by decreasing the phosphorylation of Akt, which is positively correlated with the concentration.

Autoantibodies ; China ; Cohort Studies ; Follow-Up Studies ; Humans ; Idiopathic Pulmonary Fibrosis