Expression data from control-knockdown (CTR-KD) and MAST4-KD human multiple myeloma (MM) cell lines
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ABSTRACT:
PROVIDER: PRJNA743874 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15043391_1.fastq.gz | Fastqsanger.gz | |||
| SRR15043391_2.fastq.gz | Fastqsanger.gz | |||
| SRR15043392_1.fastq.gz | Fastqsanger.gz | |||
| SRR15043392_2.fastq.gz | Fastqsanger.gz | |||
| SRR15043393_1.fastq.gz | Fastqsanger.gz |
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Project description:Macophage migration inhibitor (MIF) is important for MM resistance to proteasome inhibitors. To determine what signalling pathways are affected by MIF in MM cells, we established MIF-KO MM.1S and ARP-1 MM cell lines. Total RNAs of 2 x 106 CTR-KO and MIF-KO MM cells were extracted by RNeasy Mini Kit (Qiagen). 5-10 µg RNA samples were sent to Gene Expression and Genotyping Facility at Case Western Reserve University (Cleveland, OH) for RNA-seq followed by data analysis. We use microarray data to determine differential expression of genes in MIF-KO and CTR-KO MM cells.
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Project description:To determine what signalling pathways are affected by LILRB1 in MM cells, ARP-1 MM cell lines were transfected with lentivirus to knockdown LILRB1, injected to nsg mice, sorted from the bone marrow of NSG mice and sent for RNA-seq. Total RNAs of 2 x 10^6 CTR-KD ARP-1 cells or LILRB1-KD ARP-1 cells were extracted by RNeasy Mini Kit (Qiagen). 5-10 µg RNA samples were sent to Cancer Genomics Center at The University of Texas (Houston, TX) for RNA-seq followed by data analysis. We use the RNA-seq data to determine differential expression of genes in CTR-KD ARP-1 cells and LILRB1-KD ARP-1 cells.
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Project description:Expression data from control-knockout (CTR-KO) and MIF-KO human multiple myeloma (MM) cells
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Project description:The multiple myeloma (MM) data set (endpoints F, G, H, and I) was contributed by the Myeloma Institute for Research and Therapy at the University of Arkansas for Medical Sciences (UAMS, Little Rock, AR, USA). Gene expression profiling of highly purified bone marrow plasma cells was performed in newly diagnosed patients with MM. The training set consisted of 340 cases enrolled on total therapy 2 (TT2) and the validation set comprised 214 patients enrolled in total therapy 3 (TT3). Plasma cells were enriched by anti-CD138 immunomagnetic bead selection of mononuclear cell fractions of bone marrow aspirates in a central laboratory. All samples applied to the microarray contained more than 85% plasma cells as determined by 2-color flow cytometry (CD38+ and CD45-/dim) performed after selection. Dichotomized overall survival (OS) and eventfree survival (EFS) were determined based on a two-year milestone cutoff. A gene expression model of high-risk multiple myeloma was developed and validated by the data provider and later on validated in three additional independent data sets.
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Project description:Recent studies have delineated cancer type-specific roles of histone 3 lysine 27 (H3K27) demethylase KDM6B/JMJD3 depending on its H3K27 demethylase activity. Here we show that KDM6B is expressed in multiple myeloma (MM); and that shRNA-mediated knockdown and CRISPR-mediated knockout of KDM6B abrogate MM cell growth and survival. TNFα or bone marrow stromal cell culture supernatants induce KDM6B, which is blocked by IKKβ inhibitor MLN120B, suggesting KDM6B is regulated by NF-κB signaling in MM cells. RNA-sequencing and subsequent ChIP-qPCR analyses reveal that KDM6B is recruited to the loci of genes encoding components of MAPK signaling pathway including ELK1 and FOS, and upregulates these genes expression without affecting H3K27 methylation level. Overexpression of catalytically-inactive KDM6B activates expression of MAPK pathway-related genes, confirming its function independent of demethylase activity. We further demonstrate that downstream targets of KDM6B, ELK1 and FOS, confer MM cell growth. Our study therefore delineates KDM6B function that links NF-κB and MAPK signaling pathway mediating MM cell growth and survival, and validates KDM6B as a novel therapeutic target in MM.
2017-05-01 | GSE93395 | GEO
Project description:Multiple Myeloma (MM) is a neoplasm of plasma cells originating in the bone marrow and is the second most common blood cancer in the United States. One challenge in understanding the pathogenesis of Multiple Myeloma (MM) and improving treatment is a lack of immunocompetent mouse models. We previously developed the IL6Myc mouse that generates plasmacytomas at 100% frequency that phenotypically resemble aggressive MM. Using comprehensive genomic analysis, we found that the RNA expression patterns between tumors were somewhat heterogenous, but nonetheless resembled MMSET (multiple myeloma SET domain), an aggressive form of human myeloma with poor prognosis. Cell lines derived from the mouse tumors expressed cell-surface markers typical of MM, but also expressed BAFF-R, which is infrequently found in human MM. The cell lines also had heterogeneous responses to chemotherapeutic drugs typically used to treat human MM. Interestingly IL6Myc tumors accumulated variants in genes like those seen in human MM, as well as recurrent Ig translocations, a common characteristic of human MM. These data indicate that the IL6Myc model is a useful model for aggressive MM that can be used to develop treatment and understand how early myc expression influences disease etiology.
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Project description:Purpose: In this study we compared bone marrow-derived mesenchymal stem cells (MSC) of 6 Multiple Myeloma patients (MM-MSC) with MSC of 5 control donors with other (non) malignant diseases (CTR-MSC) to detect transciptomic alterations in RNA sequencing and to identify altered gene expression patterns. Methods: MSC were obtained from bone marrow, cultivated, analyzed by flow cytometry and underwent quality control using the 4200 TapeStation (Agilent, California, USA). Following the TrueSeq stranded protocol (Illumina, California, USA) we sequenced the RNA in a 100 bp paired-end run on the HiSeq 4000 (Illumina). Results: We detected 2174 significant DEGs (adjusted p<0.05) between MM-MSC and CTR-MSC, among which 967 were up-regulated in MM-MSC. 18 out of 50 MSigDB Hallmark gene sets were significantly enriched in MM-Act-MSC compared to CTR-MSC (FDR<0.05) including PI3K-AKT-mTOR signaling, as well as NOTCH, MYC and Inflammatory response. Conclusion: Our data provides a deeper insight into the molecular signature and function of MSC associated MM-cells and show that targeting PI3K-AKT-mTOR signaling in MSC may represent an additional therapeutic pathway in the treatment of MM-patients.
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