Objective To investigate the mechanism and cause of the inactivation of tumor suppressor gene RNF180 in prostate cancer cell line by observing the effect of 5-Aza-CdR on the RNF180 gene in prostate cancer cell line DU145. Methods MTT method was adopted to study the effect of 5-Aza-CdR(0,1,2,5,10,15 and 20μmoI/L)on the proliferation of prostate cancer cells. Western blotting,real-time PCR,and methyla-tion specific PCR(MSP)were separately used to detect the expression of RNF180 in prostate cancer cells before and after the treatment of the most suitable drug concentration(5μmoI/L). Results In a certain range,the effect of 5-Aza-CdR on the proliferation of prostate cancer cell line DU145 was increased with the increase of drug concentration and the time of drug treatment(P<0.05). After the treatment of the most suitable drug concentration,the protein and mRNA expression of RNF180 in prostate cancer cells was significantly increased(P<0.05),but the methyla-tion of the promoter region was obviously decreased. Conclusion 5-Aza-CdR can reverse the methylation status of RNF180 gene in DU145 pros-tate cancer cell line,and relieve the silencing status of RNF180gene expression.

Objective To clarify the significance of RNF180 expression in carcinogenesis and progression of prostate cancer by detection of RNF180 promoter methylation. Methods RNF180 expression was detected in human prostate cancer cell lines(PC3,LNCap,and DU145)and normal prostate cells(RWPE?1)via Western blotting,RT?PCR,methylation?specific PCR(MSP),bisulfite?sequeneing PCR(BSP),respectively, while RNF180 expression in human prostate cancer tissues and paired adjacent non?tumor tissue was detected via immunohistochemistry. Results The expressions of RNF180 mRNA and protein in prostate cancer cells were significantly lower than those in normal prostate cells(P<0.05),op?posite to what was observed for the methylation level of the RNF180 promoter. Additionally,the RNF180 expression in prostate cancer tissue was significantly lower than that in paired adjacent non?tumor tissue. Conclusion The RNF180 promoter is incompletely methylated in prostate can?cer cells,which may be a reason for the decline or silencing of RNF180 expression in cancer cells and tissues.

In order to express and purify the catalytic domain of SHP-1/SHP-2 (named as D1C and D2C respectively) and determine their kinetics, the constructed D1C and D2C plasmids were transformed into Escherichia coli BL21 and the expression was induced with IPTG. The harvested cells were suspended in extraction buffer. After sonication, the solution was applied to HPLC and the results were confirmed by SDS-PAGE. The purified peptides were further subjected to kinetic specificity study using synthetic phosphotyrosine (pY) as substrate by malachite green method and analyzed by Lineweaver-Burk plot calculation. From this study, we found D1C and D2C were expressed successfully in soluble state in Escherichia coli BL21 and purified efficiently with HPLC system. The molecular weight of D1C was 34.6 kD, and its Michaelis constant (K(m)) was 2.04 mmol catalytic constant (K(cat)) was 44.98 s(-1), specific constant (K(cat)/K(m)) was 22.05 L/(mmol x s); the molecular weigh of D2C was 35.3 kD, and its Michaelis constant (K(m)) was 2.47 mmol, catalytic constant (K(cat)) was 27.45 s(-1), specific constant (K(cat)/K(m)) was L/(mmol x s). The enzyme activity of D1C is stronger than that of D2C.
Catalytic Domain ; Chromatography, High Pressure Liquid ; Escherichia coli ; genetics ; metabolism ; Kinetics ; Plasmids ; Protein Tyrosine Phosphatase, Non-Receptor Type 11 ; genetics ; metabolism ; Protein Tyrosine Phosphatase, Non-Receptor Type 6 ; genetics ; metabolism ; Recombinant Proteins ; genetics ; metabolism

OBJECTIVE:To conduct whole process information management in PIVAS of our hospital,and to promote the work quality and efficiency of pharmacy intravenous admixture service(PIVAS). METHODS:The whole process information management in PIVAS of Tianjin medical university cancer hospital(it is called our hospital for short)was introduced in respects of prescription review,medical order disposal,the deployment of the outboard and so on. Related data were selected from PIVAS of our hospital during Jun. 2015-Feb. 2017. The effects of whole process information management in PIVAS of our hospital in May 2016 were evaluated by retrospective analysis,pre and post control research method. RESULTS:Through the application of whole process information management system,the improvement of relevant management,the functions of primary checking of medical order,drug quantity statistics,record traceability,workload account,responsible person and operation time recording were realized in the links of prescription checking,medical order processing,outboard allocation,inboard allocation,cabin checking,automatic sorting. Compared with before application,6 indexes of work efficiency were improved by 33.3%-86.1% after application(P<0.05);4 indexes of the work quality were improved by 28.6%-66.7%(P<0.05);quality index of finished product infusion was improved by 12.5%(P<0.05). CONCLUSIONS:The application of whole process information management in PIVAS can improve work quality and efficiency,and facilitate the convenience of management assessment.

Dendritic cells (DCs) comprise two functionally distinct subsets: plasmacytoid DCs (pDCs) and myeloid DCs (mDCs). pDCs are specialized in rapid and massive secretion of type I interferon (IFN-I) in response to nucleic acids through Toll like receptor (TLR)-7 or TLR-9. In this report, we characterized a CD56(+) DC population that express typical pDC markers including CD123 and BDCA2 but produce much less IFN-I comparing with pDCs. In addition, CD56(+) DCs cluster together with mDCs but not pDCs by genome-wide transcriptional profiling. Accordingly, CD56(+) DCs functionally resemble mDCs by producing IL-12 upon TLR4 stimulation and priming naïve T cells without prior activation. These data suggest that the CD56(+) DCs represent a novel mDC subset mixed with some pDC features. A CD4(+)CD56(+) hematological malignancy was classified as blastic plasmacytoid dendritic cell neoplasm (BPDCN) due to its expression of characteristic molecules of pDCs. However, we demonstrated that BPDCN is closer to CD56(+) DCs than pDCs by global gene-expression profiling. Thus, we propose that the CD4(+)CD56(+) neoplasm may be a tumor counterpart of CD56(+) mDCs but not pDCs.
Biomarkers ; metabolism ; CD56 Antigen ; genetics ; immunology ; Cell Lineage ; genetics ; immunology ; Dendritic Cells ; immunology ; metabolism ; pathology ; Gene Expression ; Hematologic Neoplasms ; genetics ; immunology ; pathology ; Humans ; Immunophenotyping ; Interferon Type I ; biosynthesis ; metabolism ; Interleukin-12 ; biosynthesis ; metabolism ; Interleukin-3 Receptor alpha Subunit ; genetics ; immunology ; Lectins, C-Type ; genetics ; immunology ; Membrane Glycoproteins ; genetics ; immunology ; Myeloid Cells ; immunology ; metabolism ; pathology ; Receptors, Immunologic ; genetics ; immunology ; Terminology as Topic ; Toll-Like Receptor 4 ; genetics ; immunology ; Toll-Like Receptor 7 ; genetics ; immunology ; Toll-Like Receptor 9 ; genetics ; immunology