Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression data of lentivirus sponge MicroRNA16 (miR16) downregulated RPMI 8226 and MMS1 multiple myeloma (MM) cell lines compared with control lentivirus sponge

ABSTRACT: Multiple myeloma is characterized by frequent chromosomal alterations. Deletion of chr 13, especially band 13q14, is commonly observed in early stages of MM, suggesting the presence of tumor suppressor genes (TSG) within this region. We sought to functionally validate the role of the microRNAs-15a/16 cluster, centered at the deleted region, as TSGs and delineate their downstream target genes in MM. Using “sponge” lentiviral vectors to competitive stably inhibit mature microRNAs in vitro and in vivo, we have documented enhanced proliferative and invasive capacity of cells with stably inhibition of miR-16. Expression profiling analysis of miR-16-deficient cells identified a large number of downstream target genes. This loss-of-function system, which mimics the 13q chromosomal deletion, provides a valuable tool to investigate their function in MM pathogenesis and their potential use as therapeutic targets.

ORGANISM(S): Homo sapiens

PROVIDER: GSE24522 | GEO | 2010/10/20

SECONDARY ACCESSION(S): PRJNA132653

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Expression data of lentivirus sponge MicroRNA16 (miR16) downregulated RPMI 8226 and MMS1 multiple myeloma (MM) cell lines compared with control lentivirus sponge

Project description:Multiple myeloma is characterized by frequent chromosomal alterations. Deletion of chr 13, especially band 13q14, is commonly observed in early stages of MM, suggesting the presence of tumor suppressor genes (TSG) within this region. We sought to functionally validate the role of the microRNAs-15a/16 cluster, centered at the deleted region, as TSGs and delineate their downstream target genes in MM. Using âspongeâ lentiviral vectors to competitive stably inhibit mature microRNAs in vitro and in vivo, we have documented enhanced proliferative and invasive capacity of cells with stably inhibition of miR-16. Expression profiling analysis of miR-16-deficient cells identified a large number of downstream target genes. This loss-of-function system, which mimics the 13q chromosomal deletion, provides a valuable tool to investigate their function in MM pathogenesis and their potential use as therapeutic targets. We used microarrays to detail the global programme of gene expression underlying miR16 downregulation, simulating the 13q- cytogenetic changes related to MM in order to identified distinct classes of up-regulated genes during this process. MM cell lines were stably tranduced and sorted with miR16 lentiviruses expressing miR downregulating sponges or control sponges, and analyzed for GEP to asses possible miR16 target genes. Cells were lysed and the RNA extraction and hybridization was peformed on Affymetrix microarrays. We sought to obtain homogeneous populations of cells and therefore collected all at the same timepoint.

2010-10-20 | E-GEOD-24522 | biostudies-arrayexpress

Expression data of lentivirus sponge Protein Arginine Methyltransferase 5 downregulated NCI-H929 cell line compared with control lentivirus sponge

Project description:Multiple myeloma is characterized by frequent chromosomal alterations. Protein Arginine Methyltransferase 5 (PRMT5) catalyzes symmetric dimethylation of arginine, a post-translational modification involved in cancer and embryonic development. We sought to functionally validate the role of PRMT5 and delineate their downstream target genes in MM. Using “sponge” lentiviral vectors to knock down PRMT5 in vitro and in vivo, we have documented enhanced apoptosis and descend proliferation of MM cells compared with control lentivirus sponge . Expression profiling analysis of PRMT5-deficient cells identified a large number of downstream target genes, which provides a valuable tool to investigate their function in MM pathogenesis and their potential use as therapeutic targets.

2020-12-06 | GSE162715 | GEO

Expression data from doxycylin-inducible miR-15a/16-1 and empty vector (EV) expression in a 13q14-\- cell line

2009-12-01 | GSE18866 | GEO

Transcription profiling of human 13q14-\- cell line expressing doxycylin-inducible miR-15a/16-1 and empty vector (EV)

Project description:Reexpression of microRNAs miR-15a/16-1 in a cell line deficient for these miRs (homozygous deletion of chromosomal region 13q14) results in the downregulation of certain mRNAs. Experiment Overall Design: A doxycyclin-inducible expression vector containing miR-15a/16-1 was transfected into CLL-I83E95 cells that are deficient for those miRs. miR-expression was induced by addition of doxycyclin to the medium, and cell were harvested 48 hours later. Labeled cRNA was hybridized to microarrays and gene expression data were compared to CLL-I83U95 stably transfected with an empty vector.

2009-12-05 | E-GEOD-18866 | biostudies-arrayexpress

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

2016-01-05 | GSE76471 | GEO

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.

2016-01-05 | E-GEOD-76471 | biostudies-arrayexpress

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

Project description:Histone deacetylases (HDACs) have emerged as therapeutic targets in multiple myeloma (MM); however, the underlying roles of each class- or isoform-HDAC have not fully clarified. The present study delineates the effect of HDAC1 suppression or inhibition in MM cells. The RNA-seq analysis here revealed that HDAC1 suppression downregulated IRF4 and PIM2, which both play a crucial role in MM cell survival and proliferation. Mechanistically, HDAC1 inhibition dampens IRF4 transcription through histone hyperacetylation and hindrance of RNA polymerase II recruitment at IRF4 locus. PIM2 is transcriptionally under direct regulation by IRF4, thereby reducing PIM2 expression after HDAC1 inhibition. PIM2 is upregulated by the stimuli from bone marrow microenvironment including IL-6 independent of IRF4 regulation in MM cells. Although these stimuli reduce the cytotoxic effect of HDAC1 inhibition in MM cells, direct blockade of PIM2 overcomes the weak point of HDAC1 inhibition. The effect of the combination of class I HDAC inhibitors with PIM inhibitors is further confirmed in vivo mouse xenograft models. Our findings provoke clinical applications of class I HDAC inhibitors in combination with PIM inhibitors against MM.

2022-09-21 | GSE193298 | GEO

Construction of a recombinant lentivirus-mediated shRNA expression vector targeting the human PSMD10 gene and validation of RNAi efficiency in RPMI?8226 multiple myeloma cells.

Project description:Multiple myeloma (MM) is one of the most common malignant blood cancers. Previous studies have reported that proteasome 26S subunit non-ATPase 10 (PSMD10) is an oncoprotein with complex roles in hepatocellular carcinoma and other malignant tumors. Notably, research on the relationship between PSMD10 and tumorigenesis of MM has rarely been reported. The present study was designed to explore the possibility of PSMD10 as a therapeutic target in the treatment of MM, and the use of RNA interference (RNAi) to determine the function PSMD10. A recombinant lentivirus-mediated short hairpin RNA (shRNA) targeting human PSMD10 mRNA was constructed and used to decrease endogenous PSMD10 expression in the MM RPMI-8226 cell line in vitro. Expression of the PSMD10-targeting shRNA in RPMI-8226 cells transduced with the recombinant vector could be tracked by observing the expression of green fluorescent protein after infection. A transient transgenic RPMI-8226 cell line was generated by transducing cells with the packaged viral particles. Western blot analysis indicated that the protein levels of PSMD10 in the PSMD10-shRNA MM cells were significantly lower than those in the cells transduced with the negative control shRNA. Notably, RT-qPCR analysis did not reveal a marked change in the PSMD10 mRNA level; thus, the knockdown effect of the PSMD10-shRNA may occur during translation. Furthermore, apoptosis of MM cells was increased by silencing PSMD10 expression. Overall, the results demonstrated that the lentivirus-mediated shRNA vector-based RNAi expression system is an efficient method to silence PSMD10 gene expression in the MM RPMI-8226 cell line. It may provide a basis to study the role of PSMD10 in tumor cells, and may be a reliable gene therapy strategy in the clinic.

| S-EPMC5561814 | biostudies-literature

The Mitochondria-Independent Cytotoxic Effect of Leflunomide on RPMI-8226 Multiple Myeloma Cell Line.

Project description:Leflunomide, an anti-inflammatory agent, has been shown to be effective in multiple myeloma (MM) treatment; however, the mechanism of this phenomenon has not been fully elucidated. The aim of the study was to assess the role of mitochondria and dihydroorotate dehydrogenase (DHODH) inhibition in the cytotoxicity of leflunomide in relation to the MM cell line RPMI 8226. The cytotoxic effect of teriflunomide-an active metabolite of leflunomide-was determined using MTT assay, apoptosis detection, and cell cycle analysis. To evaluate DHODH-dependent toxicity, the cultures treated with teriflunomide were supplemented with uridine. Additionally, the level of cellular thiols as oxidative stress symptom was measured as well as mitochondrial membrane potential and protein tyrosine kinases (PTK) activity. The localization of the compound in cell compartments was examined using HPLC method. Teriflunomide cytotoxicity was not abolished in uridine presence. Observed apoptosis occurred in a mitochondria-independent manner, there was also no decrease in cellular thiols level. Teriflunomide arrested cell cycle in the G2/M phase which is not typical for DHODH deficiency. PTK activity was decreased only at the highest drug concentration. Interestingly, teriflunomide was not detected in the mitochondria. The aforementioned results indicate DHODH- and mitochondria-independent mechanism of leflunomide toxicity against RPMI 8226 cell line.

| S-EPMC8469018 | biostudies-literature

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.

2020-07-03 | GSE153710 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data