Activated-Leukocyte Cell Adhesion Molecule ; Antigens, CD ; Carcinoma, Hepatocellular ; Cell Adhesion Molecules, Neuronal ; Fetal Proteins ; Hep G2 Cells ; Humans ; Liver Neoplasms ; RNA, Small Interfering

OBJECTIVETo investigate the expression of activated leukocyte cell adhesion molecule(ALCAM) protein in prostatic intraepithelial neoplasia and adenocarcinoma, and the relationship between ALCAM expression and clinicopathological features of prostatic carcinoma.

METHODSALCAM protein expression was evaluated in the tissues of 41 human prostatic carcinomas by using immunohistochemistry (EnVision method).

RESULTSALCAM was widely expressed in prostatic epithelia. Overexpression of ALCAM was found in most prostatic intraepithelial neoplasias and low-grade cancers, whereas a decreased expression shown in some high-grade cancers. The ALCAM protein expression in prostatic carcinoma was correlated with pathological grading. However, no correlation of ALCAM expression was found with preoperative serum prostate-specific antigen levels or clinical stages.

CONCLUSIONExpression of ALCAM is disturbed in prostatic intraepithelial neoplasia and adenocarcinoma, indicating its involvement in the development of human prostatic carcinoma.

Activated-Leukocyte Cell Adhesion Molecule ; analysis ; Adenocarcinoma ; chemistry ; pathology ; Aged ; Aged, 80 and over ; Humans ; Immunohistochemistry ; Male ; Middle Aged ; Prostatic Intraepithelial Neoplasia ; chemistry ; pathology ; Prostatic Neoplasms ; chemistry ; pathology

PURPOSE: Activated leukocyte cell adhesion molecule (ALCAM), a member of the immunoglobulin superfamily, is highly expressed on dendritic cells. ALCAM and its receptor CD6 are co-stimulatory molecules in the immunological synapse; their interaction is required for T cell activation. While atopic dermatitis (AD) is recognized as a T helper 2 (Th2)-mediated allergic disease, the role of ALCAM in its pathogenesis is unclear. METHODS: ALCAM levels were measured in the serum of AD patients and AD-induced murine model by ovalbumin treatment. We next investigated transepidermal water loss, clinical score, Th2-immune responses, skin barrier gene expression and T-cell activation using wild-type (WT) and ALCAM deficiency mice. An oxazolone-induced AD-like model was also established and analyzed using WT- and ALCAM-deficient mice. RESULTS: We found that serum ALCAM levels were elevated in pediatric AD patients as well as WT AD mice, whereas Th2-type cytokine production and AD symptoms were suppressed in ALCAM-deficient mice. In addition, CD4+ effector T-cell counts in murine skin and skin-draining lymph nodes were lower in ALCAM-deficient mice than in their WT counterparts. ALCAM deficiency was also linked to higher expression of skin barrier genes and number of lamellar bodies. CONCLUSIONS: These findings indicate that ALCAM may contribute to AD pathogenesis by meditating a Th2-dominant immune response and disrupting the barrier function of the skin.
Activated-Leukocyte Cell Adhesion Molecule ; Animals ; Dendritic Cells ; Dermatitis, Atopic ; Gene Expression ; Humans ; Immunoglobulins ; Immunological Synapses ; Lymph Nodes ; Mice ; Ovalbumin ; Skin ; T-Lymphocytes ; Water

PURPOSE: The aim of this study was to identify the adipocyte-specific gene expression patterns in chorion-derived mesenchymal stem cells during adipogenic differentiation. MATERIALS AND METHODS: Chorionic cells were isolated from the third trimester chorions from human placenta at birth and identified morphologically and by fluorescence-activated cell sorting analysis. After inducing adipogenic differentiation for 28 days, cells at days 3, 10, 21 and 28 were analyzed by Oil red O staining and RNA extraction in order to assess the expression levels of adipocyte marker genes, including CCAAT-enhancer binding protein alpha (C/EBPalpha), peroxisome proliferator-activated receptor gamma (PPARgamma), fatty acid binding protein 4 (FABP4) and Glycerol-3-phosphate dehydrogenase (GPD2). Cells not induced for differentiation were compared with the induced cells as a control group. RESULTS: Chorion-derived cells showed the same pattern as fibroblasts, and expressed CD73, CD105, and CD166 antigens, but not CD45, CD34, and HLA-DR antigens. On day 3 after differentiation, cells began to stain positively upon Oil red O staining, and continuously increased in lipid granules for 4 weeks. The expression level of C/EBPalpha increased 4.6 fold on day 3 after induction, and continued to increase for 4 weeks. PPARgamma was expressed at a maximum of 2.9 fold on day 21. FABP4 and GPD2 were significantly expressed at 4.7- and 3.0-fold, respectively, on day 21, compared to controls, and further increased thereafter. CONCLUSION: Human chorion-derived mesenchymal stem cells exhibited the sequential expression pattern of adipocyte marker genes during differentiation, corresponding to adipogenesis.
Activated-Leukocyte Cell Adhesion Molecule ; Adipocytes ; Adipogenesis ; Carrier Proteins ; Chorion ; Female ; Fibroblasts ; Flow Cytometry ; Gene Expression* ; Glycerolphosphate Dehydrogenase ; HLA-DR Antigens ; Humans* ; Mesenchymal Stromal Cells* ; Parturition ; Placenta ; PPAR gamma ; Pregnancy ; Pregnancy Trimester, Third ; RNA

cell carcinoma cell lines treated with Taxol(R), cyclosporin or cyclosporin combined with Taxol(R) using cDNA microarray. The results were as following; 1. It was useful that the appropriate concentration of Cyclosporin A and Taxol(R) used in oral squamous cell carcinoma cell line was under 1 microgram/ml and 3 microgram/ml. 2. In the experimental group in which Taxol(R) and Taxol(R) + Cyclosporin A were used, the cell growth was extremely decreased. 3. In the group in which Cyclosporin A was used, the MTT assay was rarely decreased which means the activity of succinyl dehydrogenase is remained in mitochondria but in the group in which the mixture of Cyclosporin A and Taxol(R) were used, the MTT assay was extremely decreased. 4. In the each group in which Cyclosporin A(3 microgram/ml) and Taxol(R)(1 microgram/ml) were used, the cell arrest was appeared in G2/M phase and in the group in which Taxol(R)(3 microgram/ml) was used, the cell arrest was appeared in both S phase and G2/M phase. 5. In the oral squamous cell carcinoma cell line treated with Taxol(R), several genes including ANGPTL4, RALBP1 and TXNRD1, associated with apoptosis, SUI1, MAC30, RRAGA and CTGF, related with cell growth, HUS1 and DUSP5, related with cell cycle and proliferation, ATF4 and CEBPG, associated with transcription factor, BTG1 and VEGF, associated with angiogenesis, FDPS, FCER1G, GPA33 and EPHA4 associated with signal transduction and receptor activity and AKR1C2 and UGTA10 related with carcinogenesis were detected in increased levels. The genes that showed increaced expression in the oral squamous cell carcinoma cell line treated with Cyclosporin A were CYR61, SERPINB2, SSR3 and UPA3A which are known as genes associated with cell growth, carcinogenesis, receptor activity and transcription factor. The genes expressed in the HN22 cell line treated with cyclosporin combined with Taxol(R) were ALCAM and GTSE1 associated with cancer invasiveness and cell cycle regulation.]]>
Activated-Leukocyte Cell Adhesion Molecule ; Apoptosis ; Breast Neoplasms ; Carcinogenesis ; Carcinoma, Squamous Cell ; Cell Cycle ; Cell Line ; Cyclosporine ; DNA ; DNA, Complementary ; Fungi ; Gene Expression ; Mass Screening ; Mitochondria ; Oligonucleotide Array Sequence Analysis ; Oxidoreductases ; S Phase ; Signal Transduction ; Transcription Factors ; Vascular Endothelial Growth Factor A