Anti-ICAM1 monoclonal antibody, clone Bu74

Background: Prostate cancer is one of the most common malignancies in urology, especially in developed countries. Our previous studies showed that Lanthionine synthase C-like protein 1 (LanCL1) can promote the proliferation of prostate cancer cells and protect cells from oxidative stress. Also, LanCL1 protects cells by inhibiting the JNK signaling pathway after H2O2 treatment. Materials and Methods: In our study, we analyzed the data of RNA-seq to identify the DEGs after LanCL1 overexpression. We performed a functional enrichment analysis with gene set enrichment analysis (GSEA) and a database for annotation, visualization, and integrated discovery (DAVID). We also identified the critical hub gene correlated with disease prognosis by Cox regression analysis. Results: A total of 8928 DEGs were identified. Through the analysis of GO and KEGG, we found that DEGs are significantly enriched in categories related to metabolism, cancer-related signaling pathways, and inflammation. The top 15 hub genes were then identified and ranked by degree from the protein-protein interaction network. Survival analysis showed 4 hub genes related to disease prognosis and ICAM1 expression is an independent risk factor for the prognosis. Conclusion: Our results suggest the critical genes and pathways that might play key roles after LanCL1 overexpression in prostate cancer. We also provide candidate gene targets that might play important roles in prostate cancer development.

In the body, engineered nanoparticles (NPs) may be recognized and processed by immune cells, among which macrophages play a crucial role. We evaluated the effects of selected NPs [NM-100 (TiO2), NM-110 (ZnO), NM-200 (SiO2), and NM-300 K (Ag)] on THP-1 macrophage-like cells. The cells were exposed to subcytotoxic concentrations of NPs (1-25 mu g/mL) and the expression of immunologically relevant genes (VCAM1, TNFA, CXCL8, ICAM1, CD86, CD192, and IL1B) was analyzed by RT-qPCR. The expression of selected cytokines, growth factors and surface molecules was assessed by flow cytometry or ELISA. Generation of reactive oxygen species and induction of DNA breaks were also analyzed. Exposure to diverse NPs caused substantially different molecular responses. No significant effects were detected for NM-100 treatment. NM-200 induced production of IL-8, a potent attractor and activator of neutrophils, growth factors (VEGF and IGF-1) and superoxide. NM-110 triggered a proinflammatory response, characterized by the activation of transcription factor NF-kappa B, an enhanced production of proinflammatory cytokines (TNF-alpha) and chemokines (IL-8). Furthermore, the expression of cell adhesion molecules VCAM-1 and ICAM-1 and hepatocyte growth factor (HGF), as well as superoxide production and DNA breaks, were affected. NM-300 K enhanced IL-8 production and induced DNA breaks, however, it decreased the expression of chemokine receptor (CCR2) and CD86 molecule, indicating potential immunosuppressive activity. The toxicity of ZnO and Ag NPs was probably caused by their intracellular dissolution, as indicated by transmission electron microscopy imaging. The observed effects in macrophages might further influence both innate and adaptive immune responses by promoting neutrophil recruitment via IL-8 release and enhancing the adhesion and stimulation of T cells by VCAM-1 and ICAM-1 expression.