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Microarray analysis to identify the molecular mechanisms whereby pDCs confer growth and drug resistance in MM cells

ABSTRACT: Multiple Myeloma (MM) remains incurable despite novel therapies, suggesting the need for further identification of factors mediating tumorigenesis and drug resistance. We performed microarray analysis to identify the molecular mechanisms whereby pDCs confer growth and drug resistance in MM cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE17407 | GEO | 2009/07/31

SECONDARY ACCESSION(S): PRJNA118859

REPOSITORIES: GEO

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Microarray analysis to identify the molecular mechanisms whereby pDCs confer growth and drug resistance in MM cells

Project description:Multiple Myeloma (MM) remains incurable despite novel therapies, suggesting the need for further identification of factors mediating tumorigenesis and drug resistance. We performed microarray analysis to identify the molecular mechanisms whereby pDCs confer growth and drug resistance in MM cells. Comparsion of MM cells in the presence and absence of pDCs (plasmacytoid dendritic cells)

2009-07-31 | E-GEOD-17407 | biostudies-arrayexpress

Myeloma cells via E-cadherin convert pDCs to become tumor-promoting cells

Project description:Analysis of gene expression change induced by myeloma cells in pDCs. The hypothesis tested in the present study was that myeloma cells inhibit pDCs function by direct contact. Results provide important information of gene expression change in the cocultured of pDCs and myeloma, such as IFNs and IFN regulatory genes, TLR9 signaling pathways.

2018-04-26 | GSE113647 | GEO

Homo sapiens

Project description:Microarray analysis to identify the molecular mechanisms whereby pDCs confer growth and drug resistance in MM cells

| PRJNA118859 | ENA

Ribosomal protein S3 mediates drug resistance of proteasome inhibitor: therapeutic application in multiple myeloma

Project description:Multiple myeloma (MM) remains incurable due to drug resistance. Ribosomal protein S3 (RPS3) has been identified as a non-Rel subunit of NF-κB. However, the detailed biological roles of RPS3 remain unclear. Here, we report for the first time that RPS3 is necessary for MM survival and drug resistance. RPS3 was highly expressed in MM, and knockout of RPS3 in MM inhibited cell growth and induced cell apoptosis both in vitro and in vivo. Overexpression of RPS3 mediated the proteasome inhibitor resistance of MM and delayed the survival of MM tumour-bearing animals. Moreover, our present study found an interaction between RPS3 and the thyroid hormone receptor interactor 13 (TRIP13), an oncogene related to MM tumorigenesis and drug resistance. We demonstrated that the phosphorylation of RPS3 was mediated by TRIP13 via PKCδ, which played an important role in activating the canonical NF-κB signalling and inducing cell survival and drug resistance in MM. Notably, the inhibition of NF-κB signalling by the small-molecule inhibitor targeting TRIP13, DCZ0415, was capable of triggering synergistic cytotoxicity when combined with bortezomib in drug-resistant MM. This study identifies RPS3 as a novel biomarker and therapeutic target in MM.

2023-08-18 | GSE240978 | GEO

GCF-2013-281-Sundan

Project description:Multiple Myeloma (MM) is cancer in the antibody-producing plasma cells. It comprises 1 percent of all hematological malignancies. MM is incurable and fatal. The proteasome inhibitor bortezomib has improved treatment significantly, but inherent and acquired resistance remains a problem. Glutathione (GSH) is an important red-ox buffer in eukaryotic cells. In this experiment we investigate how GSH affects bortezomib-induced gene expression changes

2014-08-01 | E-MTAB-2666 | biostudies-arrayexpress

Transcription profiling of multiple mouse myeloma (MM) cells during intra-medullary progression in the 5T2MM mouse model

Project description:Insights into mechanisms involved during intra-medullary myeloma progression could be helpful in the better understanding of this disease and in the development of new therapeutical strategies. Herein gene expression profile of multiple myeloma (MM) cells during intra-medullary progression was investigated using the 5T2MM murine model. MM-cells from 3 subsequent disease stages, quiescent, intermediate and end stage were analyzed using microarrays containing 21,492 Unigene cDNA sequences. ~ 3000 calls of differentially expressed genes were obtained. Most of these genes were silenced during tumor progression. In the early stage the MM-cells had up-regulated genes involved in bone marrow (BM) homing (CCR2, CCR5), motility (tetraspanins, 67kD laminin receptor, paxillin, zyxin, prolactin receptor), invasion (annexin II, cathepsins), adhesion (integrins, ALCAM) and cell adhesion mediated drug resistance (fibronectin). Genes involved in apoptosis (Mcl-1), plasma cell differentiation (XBP-1), angiogenesis (neuropilin-2, angiopoietin-like 4), hypoxia (HIF-1a, carbonic anhydrase 9) and in retention (CXCR4/CXCL12) and anchoring of MM-cells (laminin, collgens) in the BM were up-regulated during progressive stages. Quantative RT-PCR confirmed the trend of expression. These data provide a framework of mechanisms involved in intra-medullary myeloma progression; several genes known to be important in MM-biology are highlighted and novel candidate genes are illuminated as potentially more effective therapeutical targets.

2008-03-27 | E-MEXP-186 | biostudies-arrayexpress

Myeloma-modified adipocytes exhibit a senescent-associated secretory phenotype

Project description:Bone marrow -adipocytes (BMAs) have recently been implicated in accelerating bone metastatic cancers such as AML and breast cancer. Importantly, bone marrow adipose tissue (BMAT) expands with aging and obesity- two key risk factors in multiple myeloma (MM) disease prevalence- suggesting that BMAs influence and are influenced by myeloma cells in the marrow. Here we examined how myeloma cells affect adipocytes and provide evidence that MM cells alter adipocyte gene expression and cytokine secretion profiles, creating a “MM-associated” adipocyte (MM-adipocyte) phenotype. Our findings indicate that: (1) Multiple myeloma cells decrease BM adiposity in vitro, in myeloma animal models, and in clinical samples, (2) myeloma induces widespread gene expression and phenotypic changes in adipocytes in vitro, most notable, the induction of a senescent-like phenotype in BMAs, (3) MM-adipocytes affect myeloma cell cycle, drug sensitivity, and aggressiveness, illuminating a new driver of MM cell evolution in a drug resistant clone. We demonstrate that myeloma cells exposed to MM-adipocytes are rescued from dexamethasone-induced cell cycle arrest and have increased expression of FKBP5, a potential drug resistance gene. Our findings in patients confirm that BMAs are dynamic during myeloma disease progression (decrease during MM initiation, recover during disease remission) and that the interactions between BMAs and MM cells have previously unappreciated implications in the understanding and treatment of myeloma.

2021-03-10 | GSE140374 | GEO

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

XPO1 is a critical player for Bortezomib resistance in Multiple Myeloma: A quantitative proteomic approach

Project description:Among the blood cancers, 13% mortality is caused by Multiple myeloma (MM) type of haematological malignancy. In spite of therapeutic advances in chemotherapy treatment, still MM remains an incurable disease is mainly due to emergence of chemoresistance. At present time, FDA approved bortezomib is the first line drug for MM treatment. However, like other chemotherapy, MM patients are acquiring resistance against bortezomib. The present study aims to identify and validate bortezomib resistant protein targets in MM using iTRAQ and label free quantitative proteomic approaches. 125 differentially expressed proteins were commonly found in both approaches with similar differential expression pattern. XPO1 protein was selected for further validation as its significant high expression was observed in both iTRAQ and label free analysis. Bioinformatic analysis of these common differentially expressed proteins showed a clear cluster of proteins such as SMC1A, RCC2, CSE1, NUP88, NUP50, TPR, HSPA14, DYNLL1, RAD21 and RANBP2 being associated with XPO1. Functional studies like cell count assay, flow cytometry assay and soft agar assay proved that XPO1 knock down in RPMI 8226R cell line results in re-sensitization to bortezomib drug

2019-09-09 | PXD013859 | Pride

Treatment of MM cells with IMiDs or reducing the expression of EIF2C2 significantly affects steady-state levels of miRNAs

Project description:Lenalidomide is a therapeutically active compound that binds to E3 ubiquitin ligase recruiter cereblon (CRBN) and induces cytotoxicity. We have identified eukaryotic translation initiation factor 2 subunit C2 (EIF2C2) as a new member of CRBN-downstream binding protein that plays an important role in microRNA (miRNA) maturation and function. The treatment of immunomodulatory drug (IMiD)-sensitive multiple myeloma (MM) cells with lenalidomide altered the steady-state levels of CRBN, EIF2C2 and miRNAs and induced apoptosis. However, although the treatment of IMiD-resistant MM cells with lenalidomide altered the steady-state levels of CRBN, EIF2C2 and miRNAs, but did not massively induce apoptosis. In contrast, silencing of EIF2C2 with its small hairpin RNA significantly altered the levels of miRNAs and induced apoptosis regardless of whether those cells are sensitive or resistant to IMiDs. Therefore, EIF2C2 could be considered as a new drug target for overcoming IMiDs resistance in MM cells.

2016-03-09 | GSE61693 | GEO

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