AIM: The purpose of this study is to investigate the mechanisms related to oxidized low-density lipoprotein(ox-LDL) and dendritic cells(DCs) in the process of atherosclerosis.METHODS: Human DCs were prepared from human CD14~+ peripheral blood monocytes using rhGM-CSF((100 ?g/L)) and rhIL-4(40 ?g/L).Cells were incubated with(100 mg/L) native or oxidized LDL for 72 h.The formation of foam cells was investigated by electron microscopy and oil red O staining.Phenotypic and immune functional assays were used with FACS,FITC-dextran phagocytosis,allogeneic mixed T lymphocytes reaction and secretion of Th1/Th2(IL-12/IL-2) cytokines were also conduced.RESULTS: DCs treated with ox-LDL,but not native LDL were induced into foam cells after cultured for 72 h.Compared with native LDL,ox-LDL-treated DCs were less potent in FITC-dextran phagocytosis.ox-LDL promoted allogeneic T cells proliferation.Moreover,ox-LDL upregulated CD80(72.4? 9.6 vs 89.5?10.1,P

AIM: To investigate the effect of advanced glycosylation end products on the expression of receptor for advanced glycosylation end products in human monocyte-derived dendritic cells. METHODS: Monocytes were purified (over 98%) using anti-CD14+ microbeads. After 8 d culture in RPMI-1640 medium containing rhGM-CSF (100 ?g/L) and rhIL-4 (50 ?g/L), immature MDCs were derived, then exposed to AGE-BSA (0 or 200 mg/L) for 24 h. Expression of RAGE was semi-quantified by RT-PCR and Western blotting. At the same time, supernatants were collected. IFN-? and IL-12 were analyzed by ELISA. RESULTS: mRNA and protein of RAGE incubated by 200 mg/L AGE-BSA was higher than that in control at 24 h. Treatment of DCs with AGE-BSA resulted in about two-fold increase in the expression of RAGE (P

Purpose: NUF2 has been implicated in multiple cancers recently, suggesting NUF2 may play a role in the common tumorigenesis process. In this study, we aim to perform comprehensive meta-analysis of NUF2 expression in the cancer types included in the Cancer Genome Atlas (TCGA). Materials and Methods: RNA-sequencing data in 31 cancer types in the TCGA data and 11 independent datasets were used to examine NUF2 expression. Silencing NUF2 using targeting shRNAs in hepatocellular carcinoma (HCC) cell lines was used to evaluate NUF2’s role in HCC in vitro and in vivo. Results: NUF2 up-regulation is significantly observed in 23 out of the 31 cancer types in the TCGA datasets and validated in 13 major cancer types using 11 independent datasets. NUF2 overexpression was clinically important as high NUF2 was significantly associated with tumor stages in eight different cancers. High NUF2 was also associated with significantly poorer patient overall survival and disease-free survival in eight and six cancers, respectively. We proceeded to validate NUF2 overexpression and its negative association with overall survival at the protein level in an independent cohort of 40 HCC patients. Compared to the non-targeting controls, NUF2 knockdown cells showed significantly reduced ability to grow, migrate into a scratch wound and invade the 8 μm porous membrane in vitro. Moreover, NUF2 knockdown cells also formed significantly smaller tumors than control cells in mouse xenograft assays in vivo. Conclusion NUF2 up-regulation is a common feature of many cancers. The prognostic potential and functional impact of NUF2 up-regulation warrant further studies.