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Genome-wide mapping of chromatin state in RPMI-8226 control versus REIIBP stable overexpressing cells

ABSTRACT: Genome-wide mapping of chromatin state in RPMI-8226 control versus REIIBP stable overexpressing cells

PROVIDER: PRJNA813444 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18253368.fastq.gz	Fastqsanger.gz
	SRR18253369.fastq.gz	Fastqsanger.gz
	SRR18253370.fastq.gz	Fastqsanger.gz
	SRR18253371.fastq.gz	Fastqsanger.gz
	SRR18253372.fastq.gz	Fastqsanger.gz

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Expression data analysis from RPMI 8226 cells irraidated to C-ions.

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Expression data analysis from RPMI 8226 cells irraidated to C-ions.

Project description:Multiple Myeloma (MM) is an hematological malignancy. MM cells are resistant to X-ray irradiations. We irradiated RPMI 8226 cancer cells with C-ions, which are more energetic than X-ray irradiations. We found that MM cells, RPMI 8226, are also resistant to C-ion irradiations. We used microarrays to investigate the mechanisms of MM cell resistance to C-ion irradiations. MM cells, RPMI 8226, were subjected to 0 or 6 Gy doses of C-ion irradiations. RNA were extratred from each batch of cells one day after irradiations and subjected to microarray analysis.

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Genome-wide mapping of chromatin state in RPMI-8226 control versus REIIBP stable overexpressing cells

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Transcriptomic analysis of natural killer (NK) cells after co-culture with RPMI 8226 multiple myleoma cell line in the presence or absence of peripheral blood lymphocytes

Project description:Isatuximab is an IgG1 antibody that recognizes CD38 molecule on the surface of MM plasma cells and induces, among others, NK cell-mediated antibody-dependent cell-mediated cytotoxicity (ADCC). In this study we sough to unveil the effect of anti-CD38 antibody on NK cells We used microarrays to detail the global programme of gene expression underlying the differences among NK cells co-cultured with RPMI 8226 cells in the presence or absence of anti-CD38 antibody

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RNA-seq analysis of human multiple myeloma cell line RPMI 8226 after HDAC1 knockdown

Project description:RNA-seq analysis of human multiple myeloma cell line RPMI 8226 after HDAC1 knockdown

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Genome-scale CRISPR-Cas9 knockout screening for identification of genes which regulate CD38 expression in RPMI 8226 cells

Project description:We showed that interleukin-6 (IL-6) from bone marrow stromal cells downregulated CD38 expression in multiple myeloma (MM) cells. Then we performed a genome-scale CRISPR-Cas9 knockout screening to identify key molecules mediating IL-6-induced CD38 downregulation. Although IL-6 triggered downregulation of CD38 expression on the majority of RPMI 8226 cells, a small fraction maintained relatively high CD38 expression. We therefore sorted those top 5% cells with CD38-high expression and compared these cells with non-sorted control cells. The gene rank based on p-value identified Janus kinase (JAK) 1 and signal transducer-activator of transcription (STAT) 3 as highly positively enriched genes as potential mediators of IL-6-induced CD38 downregulation. We validated STAT3 and found CD38 expression was regulated by both STAT1 (positively) and STAT3 (negatively), and that inhibition of JAK-STAT3 pathway represents a novel therapeutic option to enhance CD38 expression and anti-CD38 monoclonal antibody-mediated MM cytotoxicity.

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Project description:In order to identify the effects of TFEB overexpression on the hela cells transcriptome, we performed Affymetrix Gene-Chip hybridization experiments for the hela TFEB stable clones Transcriptome analysis of hela stable clones overexpressing TFEB-GFP

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Genome-scale CRISPR-Cas9 knockout screening for identification of genes which regulate CD38 expression in RPMI 8226 cells

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CD20 positive cells are undetectable in the majority of multiple myeloma cell lines and are not associated with a cancer stem cell phenotype

Project description:Although new therapies have doubled the survival of multiple myeloma (MM) patients, this remains an incurable disease. It has been postulated that the so-called MM Cancer Stem Cells (MM-CSC) would be responsible for tumor initiation and relapse but their unequivocal identification remains unclear. Here, we investigated in a panel of MM cell lines the presence of CD20+ cells harboring a MM-CSC phenotype. Among the multiple cell lines investigated, only a small population of CD20dim+ cells (0.3%) in the RPMI-8226 cell line was found. CD20dim+ RPMI-8226 cells expressed the plasma cell markers CD38 and CD138 and were CD19-CD27-. Additionally, CD20dim+ RPMI-8226 cells did not exhibit stem-cell markers as shown by gene expression profiling and the aldehyde dehydrogenase (ALDH) assay. Moreover, we demonstrated that CD20dim+ RPMI-8226 cells are not essential for CB17-SCID mice engraftment and show lower self-renewal potential than the CD20- RPMI-8226 cells. These results do not support CD20+ expression for the identification of MM-CSC.

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