Drug resistance-related changes in gene expression profile in multiple myeloma
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ABSTRACT: 1) We identified the genes whose expression was up- and down-regulated by the adhesion to bone marrow stromal cells in human multiple myeloma cell line RPMI8226. 2) We identified the genes whose expression was up- and down-regulated by the PI3K inhibitor PF-04691502 in human multiple myeloma cell line RPMI8226.
Project description:1) We identified the genes whose expression was up- and down-regulated by the adhesion to bone marrow stromal cells in human multiple myeloma cell line RPMI8226. 2) We identified the genes whose expression was up- and down-regulated by the PI3K inhibitor PF-04691502 in human multiple myeloma cell line RPMI8226. We isolated mRNA from the multiple myeloma cell line RPMI8226 under drug-resistant conditions, and subjected them to gene expression profiling using an Agilent GeneChip Array.
Project description:We performed genome-wide DNA methylation profiling of KMS11, MM.1S, and RPMI8226 multiple myeloma cell lines to identify methylation changes distinct to each cell line Three multiple myeloma cell lines (KMS11, MM.1S, and RPMI8226) with two replicates each
Project description:We performed Illumina Infinium whole-genome SNP-CN profiling of KMS11, MM.1S, and RPMI8226 multiple myeloma cell lines to detect gene copy number variants distinct to each cell line Three multiple myeloma cell lines (KMS11, MM.1S, and RPMI8226)
Project description:Multiple myeloma RPMI8226 cells adapted to growth in melphalan display a shift towards Warburg metabolism and modulated oxidative stress signaling. Inhibitors targeting specific enzymes in these pathways are selectively toxic to the melphalan-resistant cells. To investigate large scale alterations in gene expression accompanying melphalan resistance, we used the multiple myeloma cell line RPMI8226 and its melphalan-resistant derivative LR5. The stable isotope labeling by amino acids in cell culture (SILAC) approach.
Project description:To identify the HAPLN1-induced genes regulated by STAT1 in multiple myeloma, we treated RPMI8226 multiple myeloma cells (WT or STAT1 KO) with recominant HAPLN1-PTR1. We then performed gene expression profiling analysis using data obtained from RNA-seq.
Project description:We performed genome-wide DNA methylation profiling of KMS11, MM.1S, and RPMI8226 multiple myeloma cell lines to identify methylation changes distinct to each cell line
Project description:In multiple myeloma (MM), abnormal plasma cells interact with bone marrow (BM) stromal cells and vascular cells among others. A part of the BM milieu is considered highly hypoxic, and myeloma cells in situ may be influenced by circumstances other than normoxia in vitro. Hence, we attempted to confirm the role of hypoxic MM-derived exosomes in the BM milieu. We established a novel hypoxia-resistant cell line, RPMI8226-HR derived from RPMI8226 cells, KMS-11-HR derived from KMS-11, U266-HR derived from U266, and IM-9-HR derived from IM-9 cultured for >4 months under hypoxia (1% O2), as a model of MM cells localizing in an extensively hypoxic milieu. We used RPMI8226 cells and RPMI8226-HR cells, as donor cells, and HUVECs as recipient cells. Exosomes derived from RPMI8226 cells (normoxia or hypoxia) and exosomes derived from RPMI8226-HR cells (hypoxia-resistant, HR sub-line) were used for validation of angiogeneic activity, such as tube formation assay. Exosomes derived from the RPMI8226-HR cells significantly increased tube formation of HUVECs than those from RPMI8226 cells.
Project description:We performed Illumina Infinium whole-genome SNP-CN profiling of KMS11, MM.1S, and RPMI8226 multiple myeloma cell lines to detect gene copy number variants distinct to each cell line
Project description:To investigate the role of HAPLN1 in multiple myeloma, we treated RPMI8226 multiple myeloma cells with recombinant HAPLN1-PTR1. We then performed gene expression profiling analysis using data obtained from RNA-seq.
Project description:The project aims at identifying surface proteins that are modified by the tetrasaccharide sialyl Lewisa/x and therefore serve as selectin ligands in Multiple Myeloma. To that end, we have performed an immunoprecipitation using the Heca452 antibody (which recognizes sialyl Lewisa/x-related structures) and a matched isotype control on membrane-enriched fractions that have been generated from the sialyl Lewisa/x-enriched and parental Multiple Myeloma cell line MM1S and RPMI8226. Using this approach, we have been able to identify candidate proteins that may function as selectin ligands in myeloma.