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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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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 Global RNA expression in tumors harvested from SCID mice and derived from either bortezomib-sensitive or bortezomib-resistant MCL cell lines

ORGANISM(S): Homo sapiens

SUBMITTER: Gael Roue

PROVIDER: E-GEOD-51371 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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

2013-10-18 | GSE51371 | GEO

Comparative study of a mTOR inhibitor, a pan-PI3K inhibitor and a dual PI3K/mTOR inhibitor in MCL

Project description:Phosphatidylinositol-3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) pathway activation contributes to mantle cell lymphoma (MCL) pathogenesis and drug resistance. However, the use of mTOR inhibitors as single agents have shown limited clinical efficacy in relation with drug activation of feedback loops. Selective PI3K inhibition or dual PI3K/mTOR catalytic inhibition are different therapeutic approaches developed to achieve effective pathway blockage. Here, we evaluated the antitumor activity of a mTOR inhibitor, a pan-PI3K inhibitor and a dual PI3K/mTOR inhibitor in primary MCL cells. We found that dual PI3K/mTOR inhibitor modulated angiogenesis, tumor invasiveness and cytokine signaling compared to a mTOR inhibitor and a pan-PI3K inhibitor in MCL. We used microarrays to compare the effect of these three compounds in MCL and identified distinct classes of down-regulated genes modulated by each compound. Global RNA expression in primary cells from two MCL patients treated with a mTOR inhibitor, a pan-PI3K inhibitor and a dual PI3K/mTOR inhibitor for 8 hours

2013-12-14 | E-GEOD-53309 | biostudies-arrayexpress

Antitumoral activity of acadesine and rituximab in MCL

Project description:Acadesine is a nucleoside analogue with known antileukemic effects in different neoplasms. We investigated the activity of acadesine ne exerts a cytotoxic effect in MCL and synergizes with rituximab supporting clinical examination of this strategy for MCL patients We used microarrays to detail the gene expression changes in acadesine-, rituximab- and combination-treated tumors. Global RNA expression in tumors treated with acadesine, rituximab and the combination in a xenograft model of MCL (Jeko-1). Tumors were collected 18 days after the initiation of the treatments.

2013-06-13 | E-GEOD-47871 | 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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MCL-1 Drives a Metabolic Dependency on Fatty Acid Oxidation in Cancer Independent of its Anti-Apoptotic Function

Project description:MCL-1 is an anti-apoptotic BCL-2 family protein essential to the survival of diverse cell types and is a major driver of cancer and chemoresistance. The unique oncogenic supremacy of MCL-1, as compared to its anti-apoptotic homologs, suggests that it has additional functions to complement apoptotic suppression. Here, we find that MCL-1-dependent hematologic cancer cells selectively rely on fatty acid oxidation (FAO) as a fuel source due to metabolic wiring enforced by MCL-1 itself. Importantly, this metabolic function is independent of anti-apoptotic activity, as demonstrated by metabolomic, proteomic, and genomic profiling of MCL-1-dependent leukemia cells lacking pro-apoptotic BAX and BAK. Genetic deletion of Mcl-1 results in selective downregulation of proteins within the FAO pathway, accompanied by cell death upon glucose deprivation despite apoptotic blockade. Our data reveal that MCL-1 drives a programmatic dependency on FAO in hematologic cancer cells, which can be effectively targeted by FAO inhibitors.

2022-10-03 | PXD031364 | Pride

SOX11 Gene Expression Profiling

Project description:The neural transcription factor SOX11 is overexpressed in aggressive lymphoid neoplasms mainly in mantle cell lymphoma (MCL), but its functional role in malignant B-cells is unknown. To identify target genes transcriptionally regulated by SOX11 in malignant lymphoid cells, we have used Gene Expression Profiling (GEP) after SOX11 silencing in MCL cell lines. Differential gene expression between Z138-shSOX11 and Z138-shControl MCL cell lines. To determine the transcriptional programs regulated by SOX11, we first generated an MCL cellular model with reduced SOX11 protein levels by infecting MCL cell lines with lentiviral particles carrying shRNA plasmids specifically targeting SOX11 (shSOX11.1 and shSOX11.3). Next, we compared the GEP of shSOX11 and shControl Z138 stable transduced clones using the Affymetrix U133+2.0 microarrays.

2013-04-04 | E-GEOD-34763 | biostudies-arrayexpress

IFITM3 BioID Interactomes in B-ALL and MCL

Project description:To determine the roles of membrane associated IFITM3 in BCR-signalling in B-cell malignancies we expressed N-terminal BirA-IFITM3-Y20E fusion or BirA-EV control in patient derived B-ALL cells (PDX2) and Jeko1 Mantle cell lymphoma (MCL) cells. Additionally to examine the role of PIP3 binding residues in the conserved intracellular loop region a K83A/K104A mutated form of IFITM3-Y20E-BirA fusion and compared with basic patch unmutated.

2020-12-18 | PXD020697 | Pride

Transcriptional responses of mantle cell lymphoma (MCL) lines to PKC inhibition

Project description:MCL lines (biological replicates) were treated with DMSO or 2.5uM Sotrastaurin for 3hrs This experiment is designed to see if a common set of genes is affected by Sotrastaurin (STN) treatment in STN-sensitive and STN-insensitive MCL lines. MCL cells were seeded in 6well dishes and treated for 3hrs with DMSO or 2.5uM Sotrastaurin

2013-12-01 | E-GEOD-42549 | biostudies-arrayexpress

Transcriptional responses of mantle cell lymphoma (MCL) lines to PKC inhibition

2013-12-01 | GSE42549 | GEO

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