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Sensitivity to proteasome inhibition and in vivo growth properties of MCL cells

ABSTRACT: MCL cells resistant to bortezomib show distinct tumor growth in vivo when compared to their bortezomib-sensitive counterpart We used microarrays to detail the factors underlying the increased tumorigenicity of bortezomib-resistant cells in vivo

ORGANISM(S): Homo sapiens

PROVIDER: GSE51371 | GEO | 2013/10/18

SECONDARY ACCESSION(S): PRJNA222845

REPOSITORIES: GEO

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Sensitivity to proteasome inhibition and in vivo growth properties of MCL cells

Project description:MCL cells resistant to bortezomib show distinct tumor growth in vivo when compared to their bortezomib-sensitive counterpart We used microarrays to detail the factors underlying the increased tumorigenicity of bortezomib-resistant cells in vivo Global RNA expression in tumors harvested from SCID mice and derived from either bortezomib-sensitive or bortezomib-resistant MCL cell lines

2013-10-18 | E-GEOD-51371 | biostudies-arrayexpress

Bortezomib resistance in Mantle Cell Lymphoma (MCL) is associated with plasmacytic differentiation

Project description:Bortezomib-induced resistant MCL cell lines (HBL2 BR and JEKO BR) were generated by continuous cultured of corresponding parental cell lines (HBL2 PT and JEKO PT) with increasing bortezomib concentrations The IC50 of bortezomib of BR cell lines was 80 fold higher than the IC50 of the parental clone for HBL2-BR and 40 fold higher for JEKO-BR.RNA was isolated from cells collected at different time points within the period of one month in triplicate for HBL2 and in duplicate for JEKO subclones. This material was used for gene expression analysis using Affymetrix platform. Keywords: RNA Comparision of gene expression profiling in matched pairs of PT and BR cell lines

2010-10-13 | E-GEOD-20915 | biostudies-arrayexpress

Bortezomib resistance in Mantle Cell Lymphoma (MCL) is associated with plasmacytic differentiation

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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

Modulation of Navitoclax Sensitivity by Dihydroarteminisin-Mediated MCL-1 Repression

Project description:Poor prognosis BCR-ABL+ B-ALL leukemic cells are highly dependent on the expression of endogenous anti-apoptotic MCL-1. However, the survival of most normal blood cells (e.g. progenitors, lymphocytes, and granulocytes) and other normal cell types (e.g. cardiomyocytes and neurons) are also exquisitely dependent on Mcl-1 gene expression, suggesting that effective therapeutic inhibition of MCL-1 could be acutely toxic, especially when combined with standard chemotherapy. Therefore, as an alternative to MCL-1 inhibition, we have identified dihydroarteminisin (DHA), a water-soluble metabolite of the anti-malarial arteminisin, which induces the down-modulation of MCL-1 protein expression by triggering an endoplasmic reticulum stress response. The DHA induced repression of MCL-1 expression renders leukemic cells highly sensitive to synergistic cell death induced by BH3-mimetic agents such as navitoclax (ABT-263) in a mouse model of BCR-ABL+ B-ALL. Furthermore, DHA also synergizes with navitoclax in human Ph+ ALL cell lines, and primary patient derived xenografts of Ph+ ALL. These data demonstrate that combining DHA with BH3-mimetic agents can improve therapeutic response in poor prognosis leukemia.

2018-02-14 | GSE95809 | GEO

PRMT5 inhibition in MCL

Project description:To identify the mechanistic underpinning of the anti-tumor activity of PRMT5 inhibition in MCL, we explored transcriptomic profiles of PDX-AA cells treated in vivo for 2 weeks with PRT-382, ibrutinib, or vehicle control (n=3/group).

2023-09-27 | GSE220936 | GEO

Thermotoga neapolitana Mcl

Project description:Thermotoga neapolitana Mcl Genome sequencing

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Transcriptomic profiling of drug-naïve or proteasome inhibitor-resistant myeloma cell lines

Project description:RNA was extracted from myeloma cell lines that were either drug-naïve or resistant to bortezomib or carfilzomib and the transcriptome was characterised using RNA sequencing.

2021-12-01 | GSE144249 | GEO

Comparison of CLL and MCL primary cells obtained from a patient with MCL variant Richter syndrome

Project description:Comparison of CLL and MCL primary cells obtained from a patient with MCL variant Richter syndrome

2016-07-13 | GSE84286 | GEO

HRP2-MINA complex reprograms t(4;14) multiple myeloma epigenome to dictate chemosensitivity to proteasome inhibitors [RNA-Seq]

Project description:Depletion of HRP2 induced remarkable resistance to PIs induced apoptosis of MM cells in vitro and in vivo, and suppressed expression of HRP2 was observed in bortezomib-resistant (BR) MM cells. Notably, HRP2 altered chemosensitivity more obviously in MM cells with t(4;14) translocation, and much remarkable resistant to PIs than other reagents. Moreover, HRP2 abolition of HRP2 augmented H3K27me3 modification, consequentially intensifying transcriptome alteration prone to cell survival and restriction of endoplasmic reticulum (ER) stress. Mechanistically, HRP2 recognized H3K36me2 and recruited the histone demethylases MYC-induced nuclear antigen (MINA) to degrade H3K27me3, released suppression on genes responsible for drug resistance, such as ATF3 and NR4A1. Thus, an EZH2 inhibitor, tazemetostat, synergistically sensitized anti-MM effect of bortezomib both in vitro and in vivo. Collectively, our study provides novel knowledge to understand the origination of chemoresistance in MM patients with t(4;14), and rationale for managing MM patients according to different genomic backgrounds.

2021-02-11 | GSE166524 | GEO

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