Effect of treatment OPM2 multiple myeloma cells with EPA, DHA or bortezomib
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ABSTRACT:
PROVIDER: PRJEB54097 | ENA |
REPOSITORIES: ENA
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Project description:OPM2 cells were seeded in a 12-well plate at density of 10 × 103 cells/well and incubated with the indicated concentrations of compounds. OPM2 cells were treated with 50 µM of DHA/EPA (6 h) or 10 nM of bortezomib (4 h). Total RNA was extracted from cells using RNeasy Mini Kit (74104, Qiagen, Hilden, Germany) and RNA integrity was determined by Agilent 2100 analysis. RNA integrity numbers (RIN) of all samples were greater than 8.0. RNA-seq libraries were prepared and sequenced at Novogene (Novogene, Cambridge, UK)
2022-06-26 | E-MTAB-11907 | biostudies-arrayexpress
Project description:MicroRNA microarray profilling analysis was performed on exosomes derived from serum in patients with myeloma in two conditions of therapeutic efficacy, Bortezomib resistance and Bortezomib response. Bortezomib is approved and widely used treating myeloma.
2016-07-31 | GSE71435 | GEO
Project description:MicroRNA microarray profilling analysis was performed on exosomes derived from serum in patients with myeloma in two conditions of therapeutic efficacy, Bortezomib resistance and Bortezomib response. Bortezomib is approved and widely used treating myeloma. Two kinds of sample were analyzed. MicroRNA microarray profilling analysis (using miRCURY LNA microRNA Array, 7th generation REV - hsa, mmu & rno, mirBase release 18, ProductNumber=208520,208521,208522) was performed on exosomes derived from serum in patients with myeloma in two conditions of therapeutic efficacy, Bortezomib resistance and Bortezomib response.
2016-07-31 | E-GEOD-71435 | biostudies-arrayexpress
Project description:To confirm changing C2C12 cells genetic profile and losing their myogenic ability, we investigated the combined effect of EPA and DHA on the relative expression of genes regulating the terminal differentiation of myoblast into mature multinucleated myotubes.
2020-06-24 | PXD016929 | Pride
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.
2014-03-13 | GSE55818 | GEO
Project description:RNA was extracted from myeloma cell lines which were made engraftable and resistant to bortezomib and the transcriptome was characterised using RNA sequencing.
2023-12-10 | GSE235288 | GEO
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
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
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.
2010-02-15 | GSE11866 | GEO
Project description:Gene expression profile (GEP) was analyzed from cultured bone marrow (BM) samples from patients with bortezomib responsive versus bortezomib resistant myeloma after 6-8 hours incubation in vitro with bortezomib 2 µg/ml or with PBS. Case D also had a fresh BM sample taken 75 minutes after IV injection of bortezomib.
2013-11-01 | GSE51940 | GEO