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The oligosaccharyltransferase complex is an essential component of multiple myeloma plasma cells that regulates bortezomib resistance

ABSTRACT: The oligosaccharyltransferase complex is an essential component of multiple myeloma plasma cells that regulates bortezomib resistance

PROVIDER: PRJNA1120860 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29309529_1.fastq.gz	Fastqsanger.gz
	SRR29309529_2.fastq.gz	Fastqsanger.gz
	SRR29309530_1.fastq.gz	Fastqsanger.gz
	SRR29309530_2.fastq.gz	Fastqsanger.gz
	SRR29309531_1.fastq.gz	Fastqsanger.gz

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The oligosaccharyltransferase complex is an essential component of multiple myeloma plasma cells that regulates bortezomib resistance

Project description:Multiple myeloma (MM) is an incurable malignancy characterized by mutated plasma cell clonal expansion in the bone marrow, leading to severe clinical symptoms. Thus, identifying new therapeutic targets for MM is crucial. We identified the oligosaccharyltransferase (OST) complex as a novel vulnerability in MM cells. Elevated expression of this complex is associated with relapsed, high-risk MM, and poor prognosis. Disrupting the OST complex suppressed MM cell growth, inducing cell cycle arrest and apoptosis. Combined inhibition with bortezomib synergistically eliminated MM cells in vitro and in vivo, via suppressing genes related to bortezomib-resistant phenotypes. Mechanistically, OST complex disruption downregulated pathological gene signatures (NF-kB signaling, mTORC1 pathway, glycolysis, MYC targets, and cell cycle), induced TRAIL-mediated apoptosis and inflammatory pathways. MYC translation was robustly suppressed upon inhibiting the OST complex. Collectively, the OST complex presents a novel target for MM treatment, and combining its inhibition with bortezomib offers a promising approach for relapsed MM patients.

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MicroRNA Expression Profile of serum exosomes from Bortezomib-resistant and Bortezomib-response patients in multiple myeloma

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A Subset of Genes Can Distinguish between Bortezomib Responsive Versus Bortezomib Resistant Myeloma

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.

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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.

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

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An orthotopic syngeneic mouse model of bortezomib-resistant multiple myeloma

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.

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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.

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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

Targeting the RBM39-MEK5 axis synergizes with bortezomib to inhibit the malignant growth of multiple myeloma

Project description:Targeting the RBM39-MEK5 axis synergizes with bortezomib to inhibit the malignant growth of multiple myeloma

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