Unknown,Transcriptomics,Genomics,Proteomics

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Expression profiling MOLT-4 treated with MABL

ABSTRACT: Analysis of MOLT-4 cells at various time points up to 6 hours following treatment with mouse anti-CD47 antibody (MABL) and goat anti-mouse IgG (GAM) as the crosslinker of MABL. MABL induces apoptosis in CD47-positive MOLT-4 cells. Cell death signals via CD47 ligation were analyzed by using Affymetrix Human Genome U133A microarray. MOLT-4 cell line was obtained from the American Type Culture Collection (ATCC) and grown in RPMI1640 medium (SIGMA) with 10% FBS(JBS). It was maintained at 37 degree C and 5% CO2. Cells were washed with PBS(-) followed by treatment with 10 ug/mL MABL (anti-CD47 antibody) for 0, 0.5, 1, 3 and 6 h. Total RNA was isolated and converted to cDNA using a Superscript Double Stranded cDNA synthesis kit (Invitrogen). Fragmented cDNA was hybridized to Affymetrix Human Genome U133A array and gene expression signals were analyzed. Probes showing >2 or <0.5 fold-change for both replicates compared with the control (geometric mean of 0h replicate signals) were selected at any time.

ORGANISM(S): Homo sapiens

SUBMITTER: Naoshi Fukushima

PROVIDER: E-GEOD-16494 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Intercellular communication is critical for integrating complex signals in multicellular eukaryotes. Vascular endothelial cells and T lymphocytes closely interact during the recirculation and trans-endothelial migration of T cells. In addition to direct cell-cell contact, we show that T cell derived extracellular vesicles can interact with endothelial cells and modulate their cellular functions. Thrombospondin-1 and its receptor CD47 are expressed on exosomes/ectosomes derived from T cells, and these extracellular vesicles are internalized and modulate signaling in both T cells and endothelial cells. Extracellular vesicles released from cells expressing or lacking CD47 differentially regulate activation of T cells induced by engaging the T cell receptor. Similarly, T cell-derived extracellular vesicles modulate endothelial cell responses to vascular endothelial growth factor and tube formation in a CD47-dependent manner. Uptake of T cell derived extracellular vesicles by recipient endothelial cells globally alters gene expression in a CD47-dependent manner. CD47 also regulates the mRNA content of extracellular vesicles in a manner consistent with some of the resulting alterations in target endothelial cell gene expression. Therefore, the thrombospondin-1 receptor CD47 directly or indirectly regulates intercellular communication mediated by the transfer of extracellular vesicles between vascular cells. Treatment with B6H12 antibody inhibited co-immunoprecipitation of EGFR with CD47 and inhibited EGF-induced EGFR tyrosine phosphorylation. B6H12 treatment of bCSC also suppressed asymmetric cell division and cell proliferation and up-regulated caspase 3/7 activity. Correspondingly, caspase-7 cleavage in human breast cancers correlated with CD47 expression. Our data shows that B6H12 specifically targets bCSCs but not differentiated cancer cells, and this CD47 signaling is independent of SIRPÎ±. Three replicates of each condition were generated. Three replicates of each MDA-231 attached cells (differentiated), MDA-231 in suspension cells (bCSC), MDA-231 in suspension cells (bCSC) treated with Control Antibody and MDA-231 in suspension cells (bCSC) treated with B6H12 Antibody.

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Expression profiling MOLT-4 treated with MABL

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