Expression of MUC1 mucin in human umbilical vein endothelial cells (HUVEC).

Mucin 1 (MUC1) is a membrane-bound glycoprotein that is expressed by various epithelial cell types. MUC1 functions include modulation of cell adhesion, signal transduction, lubrication and hydration of epithelial surfaces, and their protection from infection. In this study we demonstrated that MUC1 is expressed in human umbilical vein endothelial cells (HUVECs) and could be released/shed from cellular membrane. MUC1 presence in these cells was verified using three methods: Western blotting, flow cytometry and metabolic labeling. We also showed that mucin expression is stimulated by proinflammatory cytokines: about a 2-fold increase was observed after TNF-Îą treatment and lower after IFN-Îł alone and in combination with TNF-Îą treatment. It can be assumed that the presence of MUC1 in endothelial cells may have an important role in the interactions with different cell types in physiological and pathological processes

Cytotoxic efficacy of a novel dinuclear platinum(II) complex used with anti-MUC1 in human breast cancer cells

Mucin 1 (MUC1) is overexpressed in various cancer cells especially in breast cancer cells. There are known research works on the use of anti-MUC1 antibody with docetaxel in ovarian cancer, but there are no data about combined therapy platinum compounds with anti-MUC1 in breast cancer. The aim of the study was to evaluate the antiproliferative properties of a new dinuclear platinum(II) complex (Pt12) used with anti-MUC1 in human breast cancer cells. The dinuclear platinum(II) complex (Pt12) has been synthesized, and its cytotoxicity with anti-MUC1 has been tested in both MCF-7 and MDA-MB-231 breast cancer cells. In this study, the effects of Pt12 with anti-MUC1 on collagen and DNA biosynthesis in human breast cancer cells were compared to those evoked by cisplatin and cisplatin with anti-MUC1. The mechanism of action of Pt12 with anti-MUC1 was studied employing flow cytometry assessment of annexin V binding assay. It was found that Pt12 with anti-MUC1 was more active inhibitor of DNA and collagen synthesis as well more cytotoxic agent than Pt12 alone and cisplatin with anti-MUC1. Cytotoxicity of Pt12 with anti-MUC1 against breast cancer cells is due to apoptotic cell death as well as necrotic cell death. These results indicate that the use of Pt12 with anti-MUC1 may constitute a novel strategy in the chemotherapy of breast cancer tumors

The participation of ribosome-UDP-GalNAc complex in the initiation of protein glycosylation in vitro

The gastric epithelial cells ribosome-UDP-GalNAc complex is a donor of UDP- GalNAc as the substrate for N-acetylgalactosaminyltransferase, which catalyse the transfer of GalNAc residue to the polypeptide, existing on polysomes. It was observed that the deglycosylated porcine mucin and synthetic peptide (PTSSPIST) can be also glycosylated with participation of N-acetylgalactosaminyltransferase and ribosome- UDP-GalNAc complex. The probability of the ribosome-UDP-GalNAc complex as an intermediate in the O-glycosylation is considered

Glutathione reductase activity correlates with concentration of extracellular matrix degradation products in synovial fluid from patients with joint diseases

The mechanisms underlying cartilage matrix degradation in joint diseases is not fully understood but reactive oxygen species are implicated as main causative factors. Comparative studies of glutathione reductase (GR) activity in synovial fluid from patients with rheumatoid arthritis (RA), reactive arthritis (ReA) and osteoarthritis (OA) as well as correlations between GR activity and concentration of the major cartilage components in synovial fluid are presented in this study. We found significantly higher activity of GR in RA (about three-fold) and ReA (about two-fold) than in OA. In RA and ReA patients, GR activity in synovial fluid correlates negatively with the concentrations of collagen and degradation products of sulfated glycosaminoglycans. In OA patients the activity of GR was significantly lower than in RA and ReA, which positively correlated with the concentration of collagen and showed a tendency for positive correlation with the degradation products of sulfated glycosaminoglycans. Our results suggest that in RA and ReA patients increased activity of GR does not prevent the increased degradation of collagen and proteoglycans by ROS

Expression of MUC1 mucin in human umbilical vein endothelial cells (HUVEC).

Mucin 1 (MUC1) is a membrane-bound glycoprotein that is expressed by various epithelial cell types. MUC1 functions include modulation of cell adhesion, signal transduction, lubrication and hydration of epithelial surfaces, and their protection from infection. In this study we demonstrated that MUC1 is expressed in human umbilical vein endothelial cells (HUVECs) and could be released/shed from cellular membrane. MUC1 presence in these cells was verified using three methods: Western blotting, flow cytometry and metabolic labeling. We also showed that mucin expression is stimulated by proinflammatory cytokines: about a 2-fold increase was observed after TNF-Îą treatment and lower after IFN-Îł alone and in combination with TNF-Îą treatment. It can be assumed that the presence of MUC1 in endothelial cells may have an important role in the interactions with different cell types in physiological and pathological processes

The levels of sMUC-1 in patients with multiple myeloma

Mucins have been shown to be aberrantly overexpressed in various diseases including cystic fibrosis, asthma, and cancer. Recent studies have uncovered the roles of these mucins in the pathogenesis of cancer. The presence of MUC-1 has also been detected on the cell surface of multiple myeloma (MM) cells in peripheral blood and showed direct correlation with tumor mass. In this study, we evaluated the levels of soluble MUC-1 (sMUC-1) in 50 new MM patients and correlated this with the levels of sMUC-1 after treatment. High levels of sMUC-1 were found in 20/50 (40%) MM patients, and in 2/50 (4%) healthy individuals (p = 0.001). According to the ISS, we found significant differences of mean sMUC-1 levels between the first stage of the disease (0.63 ± ± 0.26) and the third (0.93 ± 0.24; p = 0.03), but not with the second stage (0.80 ± 0.22; p = 0.08). Our study confirmed the correlation between elevated sMUC-1 and high elevated lactate dehydrogenase (p = 0.03) and the level of IgG in groups of patients with MM IgG at every stage of disease (p = 0.001). We showed for the first time that levels of sMUC-1 after treatment, in a group of patients with initially elevated levels of MUC-1, were statistically lower than in a group of patients with initially lower levels of sMUC-1 (21% vs. 42,6%; p = 0.05). At 37 months median of follow-up, we found a statistically significant difference between patients with normal versus elevated sMUC-1 in terms of progression-free survival (median 12 months vs. 8.1 months; p = 0.03). (<i>Folia Histochemica et Cytobiologica 2011; Vol. 49, No. 4, pp. 654–658</i>