ArticleMolecular cancer2010
Bone marrow stromal cells from multiple myeloma patients uniquely induce bortezomib resistant NF-kappaB activity in myeloma cells.
Article in Molecular cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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Who cites it
64 citing papers in PubMed, 117 citations in OpenAlex.
- Article
- Pathways to therapy resistance: The sheltering effect of the bone marrow microenvironment to multiple myeloma cells.Heliyon · 2024Review
- The bone ecosystem facilitates multiple myeloma relapse and the evolution of heterogeneous drug resistant disease.Nature communications · 2024Article
- Targeting of mitochondrial fission through natural flavanones elicits anti-myeloma activity.Journal of translational medicine · 2024Article
- Advancements in microenvironment-based therapies: transforming the landscape of multiple myeloma treatment.Frontiers in oncology · 2024Review
- Factors determining the sensitivity to proteasome inhibitors of multiple myeloma cells.Frontiers in pharmacology · 2024Review
- A prognostic model incorporating inflammatory cells and cytokines for newly diagnosed multiple myeloma patients.Clinical and experimental medicine · 2023Article
- Simultaneously Targeting Two Coupled Signalling Molecules in the Mesenchymal Stem Cell Support Efficiently Sensitises the Multiple Myeloma Cell Line H929 to Bortezomib.International journal of molecular sciences · 2023Article
- Review on Bortezomib Resistance in Multiple Myeloma and Potential Role of Emerging Technologies.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Metabolic changes underlying drug resistance in the multiple myeloma tumor microenvironment.Frontiers in oncology · 2023Article
- Mesenchymal stem/stromal cells- a principal element for tumour microenvironment heterogeneity.Frontiers in immunology · 2023Review
- A Hyaluronan and Proteoglycan Link Protein 1 Matrikine: Role of Matrix Metalloproteinase 2 in Multiple Myeloma NF-κB Activation and Drug Resistance.Molecular cancer research : MCR · 2022Article
- Timelapse viability assay to detect division and death of primary multiple myeloma cells in response to drug treatments with single cell resolution.Integrative biology : quantitative biosciences from nano to macro · 2022Article
- Targeting the Non-Canonical NF-κB Pathway in Chronic Lymphocytic Leukemia and Multiple Myeloma.Cancers · 2022Article
- A drug repurposing strategy for overcoming human multiple myeloma resistance to standard-of-care treatment.Cell death & disease · 2022Article
- GAS6/TAM signaling pathway controls MICA expression in multiple myeloma cells.Frontiers in immunology · 2022Article
- Therapeutics to harness the immune microenvironment in multiple myeloma.Cancer drug resistance (Alhambra, Calif.) · 2022Review
- Fc-engineering significantly improves the recruitment of immune effector cells by anti-ICAM-1 antibody MSH-TP15 for myeloma therapy.Haematologica · 2021Article
- COX2 confers bone marrow stromal cells to promoting TNFα/TNFR1β-mediated myeloma cell growth and adhesion.Cellular oncology (Dordrecht, Netherlands) · 2021Article
- The Role of Marrow Microenvironment in the Growth and Development of Malignant Plasma Cells in Multiple Myeloma.International journal of molecular sciences · 2021Review
4 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundComponents of the microenvironment such as bone marrow stromal cells (BMSCs) are well known to support multiple myeloma (MM) disease progression and resistance to chemotherapy including the proteasome inhibitor bortezomib. However, functional distinctions between BMSCs in MM patients and those in disease-free marrow are not completely understood. We and other investigators have recently reported that NF-kappaB activity in primary MM cells is largely resistant to the proteasome inhibitor bortezomib, and that further enhancement of NF-kappaB by BMSCs is similarly resistant to bortezomib and may mediate resistance to this therapy. The mediating factor(s) of this bortezomib-resistant NF-kappaB activity is induced by BMSCs is not currently understood.
resultsHere we report that BMSCs specifically derived from MM patients are capable of further activating bortezomib-resistant NF-kappaB activity in MM cells. This induced activity is mediated by soluble proteinaceous factors secreted by MM BMSCs. Among the multiple factors evaluated, interleukin-8 was secreted by BMSCs from MM patients at significantly higher levels compared to those from non-MM sources, and we found that IL-8 contributes to BMSC-induced NF-kappaB activity.
conclusionsBMSCs from MM patients uniquely enhance constitutive NF-kappaB activity in MM cells via a proteinaceous secreted factor in part in conjunction with IL-8. Since NF-kappaB is known to potentiate MM cell survival and confer resistance to drugs including bortezomib, further identification of the NF-kappaB activating factors produced specifically by MM-derived BMSCs may provide a novel biomarker and/or drug target for the treatment of this commonly fatal disease.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.