Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Roles of Iron in Chemoresistance of Multiple Myeloma Depends on the Interaction with Bone Marrow Stromal Cells [coculture]

ABSTRACT: To investigate the role of coculture treatment of multiple myeloma cells to bortezomib drug resistance, multiple myeloma cells were cocultured with bone marrow mesechymal stem cells

ORGANISM(S): Homo sapiens

PROVIDER: GSE214767 | GEO | 2022/10/07

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Roles of Iron in Chemoresistance of Multiple Myeloma Depends on the Interaction with Bone Marrow Stromal Cells [treatment]

Project description:To investigate the role of iron(FeAc) on bortezomib-induced drug resistance of multiple myeloma cells, we administrated MM.1S with iron and bortezomib

2022-10-07 | GSE214766 | GEO

Syntrophic coculture of Syntrophobacter fumaroxidans MPOBT and Geobacter sulfurreducens PCA

Project description:Propionate accumulation is an important bottleneck for anaerobic degradation of organic matter. We hypothesized that propionate conversion by a novel coculture of Syntrophobacter fumaroxidans and Geobacter sulfurreducens can be an alternative strategy for propionate oxidation coupled to Fe(III) reduction. In this study, we successfully cocultured S. fumaroxidans and G. sulfurreducens on propionate and Fe(III). Proteomic analyses of this coculture provided insights into the underlying mechanisms of propionate metabolism pathway and interspecies electron transfer mechanism. Our study can be further useful in understanding syntrophic propionate degradation in bioelectrochemical and anaerobic digestion systems.

2022-02-17 | PXD027104 | Pride

Down-regulation of CD9 by methylation decreased bortezomib sensitivity in multiple myeloma

2014-03-13 | GSE55818 | GEO

Bortezomib and Filgrastim to Promote Stem Cell Mobilization in Patients With Non-Hodgkin Lymphoma or Multiple Myeloma

Project description:This clinical trial studies peripheral blood hemapoietic stem cell mobilization with the combination of bortezomib and G-CSF (filgrastim) in multiple myeloma and non-Hodgkin lymphoma patients.

| 2158857 | ecrin-mdr-crc

Jumonji Demethylase Inhibitor GSK-J4 treated Multiple Myeloma JJN3 and RPMI

Project description:Analysis of Multiple Myeloma Cell lines JJN-3 and RPMI gene expression following treated with GSK-J4 or Bortezomib Total RNA extracted from cells after 6 or 24 hour treatment with either GSK-J4, GSK-J5, Bortezomib or vehicle

2016-08-21 | E-GEOD-60600 | biostudies-arrayexpress

Jumonji Demethylase Inhibitor GSK-J4 treated Multiple Myeloma JJN3 and RPMI

Project description:Analysis of Multiple Myeloma Cell lines JJN-3 and RPMI gene expression following treated with GSK-J4 or Bortezomib

2016-08-21 | GSE60600 | GEO

Down-regulation of CD9 by methylation decreased bortezomib sensitivity in multiple myeloma

Project description:Bortezomib therapy has been proven successful for the treatment of relapsed and/or refractory multiple myeloma (MM). However, both intrinsic and acquired resistance has already been observed. In this study, we explored the relationship between CD9 expression and bortezomib sensitivity in MM Both intrinsic and acquired resistance has already been observed. In this study, we explored the relationship between CD9 expression and bortezomib sensitivity in MM. We found that down-regulation of CD9 by methylation decreased bortezomib sensitivity in multiple myeloma. A six chip study using total RNA recovered from three separate wild-type cultures of U266 cells and three separate cultures of U266 with CD9 overexpression. Each chip measures the expression level of 45,033 genes from Homo sapiens with fourteen 60-mer probe pairs (PM/MM) per gene, with three-fold technical redundancy.

2014-03-13 | E-GEOD-55818 | biostudies-arrayexpress

Bortezomib inhibits mTOR pathway in multiple myeloma cells via induced expression of REDD1.

Project description:The combination of bortezomib and dexamethasone should become the reference induction treatment for multiple myeloma patients younger than 65 years. Pharmacogenomic profiles of genes involved in response to treatment may help to understand resistance. We performed gene expression profiling in 9 myeloma cell lines, incubated or not with bortezomib and dexamethasone for 6 hours. Supervised analysis identified significantly up regulated genes involved in stress responses. We focused on REDD1 a gene known to be rapidly induced by a wide variety of stress conditions and DNA damages. REDD1 expression was early and highly induced after bortezomib exposure. REDD1 induction was associated with the dephosphorylation of P70 S6 ribosomal kinase (P70S6K), a key substrate of mTOR. These effects were dependent upon cell line. REDD1 was overexpressed within two hours in bortezomib resistant cell lines in association with a cell size decrease. In sensitive cell lines, neither REDD1 induction nor morphological changes occurred. RNA interference mediated inhibition of REDD1 induction abrogates P70S6K dephosphorylation, early transitory cell size reduction and enhances sensitivity to bortezomib - dexamethasone. Our results suggest that mTOR regulation could be a resistance mechanism mediated by REDD1 expression in myeloma cells. Nine cell lines of multiple myeloma studied, incubated or not with bortezomib and dexamethasone, examined with spotted cDNA nylon membrane. Cell line and Code : JJN3 = Vel_1x; L363 = Vel_2x; LP1 = Vel_3x; MDN = Vel_4x; NCI = Vel_5x; RPMI = Vel_6x; SBN = Vel_7x; U266 = Vel_8x; XG1 = Vel_9x.

2010-02-14 | E-GEOD-11866 | biostudies-arrayexpress

Transcription profiling of human samples from multiple myeloma patients treated with bortezomib or dexamethasone

Project description:The aims of this study were to assess the feasibility of prospective pharmacogenomics research in multicenter international clinical trials of bortezomib in multiple myeloma and to develop predictive classifiers of response and survival with bortezomib. Patients with relapsed myeloma enrolled in phase 2 and phase 3 clinical trials of bortezomib and consented to genomic analyses of pretreatment tumor samples. Bone marrow aspirates were subject to a negative-selection procedure to enrich for tumor cells, and these samples were used for gene expression profiling using DNA microarrays. Data quality and correlations with trial outcomes were assessed by multiple groups. Gene expression in this dataset was consistent with data published from a single-center study of newly diagnosed multiple myeloma. Response and survival classifiers were developed and shown to be significantly associated with outcome via testing on independent data. The survival classifier improved on the risk stratification provided by the International Staging System. Predictive models and biologic correlates of response show some specificity for bortezomib rather than dexamethasone. Informative gene expression data and genomic classifiers that predict clinical outcome can be derived from prospective clinical trials of new anticancer agents. Experiment Overall Design: Purified myeloma samples were collected prior to enrolment in clinical trials of bortezomib (PS-341). Samples were subject to replicate gene expression profiling using the Affymetrix 133A/B microarray. Data was normalized in MAS5.0 and the median of replicates is reported. Data was normalized to a Ttimmed mean of 15o and is NOT log transformed. Various patient parameters are reported as well as response, TTP and survival upon treatment with bortezomib or dexamethasone.

2008-06-17 | E-GEOD-9782 | biostudies-arrayexpress

Tight Junction Protein 1 is a Modulator and Biomarker of Proteasome Inhibitor Sensitivity in Multiple Myeloma

Project description:Proteasome inhibitors are important chemotherapeutics in the treatment of multiple myeloma, but they are currently used empirically as no markers of sensitivity have been validated. We have identified expression of tight junction protein (TJP) 1 as being associated with sensitivity of plasma cells in vitro and in vivo to proteasome inhibitors. TJP1 suppressed expression of genes in the major histocompatibility class II region, including two catalytically active immunoproteasome subunits, thereby decreasing proteasome activity, a critical determinant of proteasome inhibitor sensitivity. This occurred through suppression by TJP1 of signaling through the epidermal growth factor receptor/Janus kinase 1/signal transducer and activator of transcription 3 pathway. In the clinic, high TJP1 expression in myeloma patients was associated with a significantly higher likelihood of responding to bortezomib, and with a longer time-to-progression after treatment. Taken together, these data support the use of TJP1 as a biomarker of sensitivity and resistance to proteasome inhibitors. To further elucidate mechanisms of bortezomib resistance, we developed human-derived multiple myeloma cell lines with a 4-fold or greater resistance to bortezomib. Then total RNA for bortezomib resistant (BR) and wild type (WT) was extracted and used for comparison by gene expression profiling.

2015-12-31 | E-GEOD-52369 | biostudies-arrayexpress

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