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Transcriptomic signature induced in bone marrow Mesenchymal Stem/Stromal Cells (MSC) after interaction with malignant multiple myeloma cells: implications in myeloma progression.

ABSTRACT: Mesenchymal stem/stromal cells (MSCs) derived from the BM of healthy donors (dMSCs) and myeloma patients (pMSCs) were co-cultured with the model myeloma cell line - MM.1S -, and the gene expression profile of MSCs induced by this interaction was analyzed using high density oligonucleotide microarrays. Deregulated genes in co-culture common to both d/pMSCs revealed functional involvement in tumor microenvironment cross-talk, myeloma growth induction and drug resistance, angiogenesis and signals for osteoclast activation and inhibition of osteoblasts. Additional genes induced by co-culture were exclusively deregulated in pMSCs and were predominantly associated to RNA processing, the ubiquitine-proteasome pathway, regulation of cell cycle and Wnt signaling.

ORGANISM(S): Homo sapiens

PROVIDER: GSE46053 | GEO | 2014/11/23

SECONDARY ACCESSION(S): PRJNA197142

REPOSITORIES: GEO

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Project description:The paper describes a model of multiple myeloma. Created by COPASI 4.26 (Build 213) This model is described in the article: A mathematical model of cell equilibrium and joint cell formation in multiple myeloma M.A. Koenders, R. Saso Journal of Theoretical Biology 390 (2016) 73–79 Abstract: In Multiple Myeloma Bone Disease healthy bone remodelling is affected by tumour cells by means of paracrine cytokinetic signalling in such a way that osteoclast formation is enhanced and the growth of osteoblast cells inhibited. The participating cytokines are described in the literature. Osteoclast-induced myeloma cell growth is also reported. Based on existing mathematical models for healthy bone remo- delling a three-way equilibrium model is presented for osteoclasts, osteoblasts and myeloma cell populations to describe the progress of the illness in a scenario in which there is a secular increase in the cytokinetic interactive effectiveness of paracrine processes. The equilibrium state for the system is obtained. The paracrine interactive effectiveness is explored by parameter variation and the stable region in the parameter space is identified. Then recently-discovered joint myeloma–osteoclast cells are added to the model to describe the populations inside lytic lesions. It transpires that their presence expands the available parameter space for stable equilibrium, thus permitting a detrimental, larger population of osteoclasts and myeloma cells. A possible relapse mechanism for the illness is explored by letting joint cells dissociate. The mathematics then permits the evaluation of the evolution of the cell populations as a function of time during relapse. To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models . To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information.

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Transcriptomic signature induced in bone marrow Mesenchymal Stem/Stromal Cells (MSC) after interaction with malignant multiple myeloma cells: implications in myeloma progression.

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