ArticleBlood2011
Gfi1 expressed in bone marrow stromal cells is a novel osteoblast suppressor in patients with multiple myeloma bone disease.
Article in Blood, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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Who cites it
59 citing papers in PubMed, 94 citations in OpenAlex.
- An odyssey of monoclonal gammopathies: focusing on precursors and the progression from MGUS and SMM to multiple Myeloma, with a brief overview of novel therapeutic strategies.Clinical and experimental medicine · 2026Review
- Mechanistic insights into bone destruction in multiple myeloma: Cellular and molecular perspectives.Journal of bone oncology · 2025Review
- Knockdown of Gfi1 increases BMSCs exosomal miR-150-3p to inhibit osteoblast ferroptosis in steroid-induced osteonecrosis of the femoral head through BTRC/Nrf2 axis.Endocrine journal · 2025Article
- LILRB4 on multiple myeloma cells promotes bone lesion by p-SHP2/NF-κB/RELT signal pathway.Journal of experimental & clinical cancer research : CR · 2024Article
- Long non-coding RNA H19 mediates osteogenic differentiation of bone marrow mesenchymal stem cells through the miR-29b-3p/DKK1 axis.Journal of cellular and molecular medicine · 2024Article
- Article
- Molecular Features of the Mesenchymal and Osteoblastic Cells in Multiple Myeloma.International journal of molecular sciences · 2022Review
- Epigenetic Crosstalk between Malignant Plasma Cells and the Tumour Microenvironment in Multiple Myeloma.Cancers · 2022Review
- Runx2 Deficiency in Osteoblasts Promotes Myeloma Resistance to Bortezomib by Increasing TSP-1-Dependent TGFβ1 Activation and Suppressing Immunity in Bone Marrow.Molecular cancer therapeutics · 2022Article
- LncRNA ORLNC1 Promotes Bone Marrow Mesenchyml Stem Cell Pyroptosis Induced by Advanced Glycation End Production by Targeting miR-200b-3p/Foxo3 Pathway.Stem cell reviews and reports · 2021Article
- Pathogenesis and treatment of multiple myeloma bone disease.The Japanese dental science review · 2021Review
- Myeloma Bone Disease: The Osteoblast in the Spotlight.Journal of clinical medicine · 2021Review
- The pathogenesis of bone metastasis in solid tumors: a review.Croatian medical journal · 2021Review
- Myeloma Bone Disease: A Comprehensive Review.International journal of molecular sciences · 2021Review
- Bone Marrow Mesenchymal Stromal Cells in Multiple Myeloma: Their Role as Active Contributors to Myeloma Progression.Cancers · 2021Review
- TAK1 is a pivotal therapeutic target for tumor progression and bone destruction in myeloma.Haematologica · 2021Article
- Review
- Animal Models of Multiple Myeloma Bone Disease.Frontiers in genetics · 2021Review
- Prevalence of the GFI1-36N SNP in Multiple Myeloma Patients and Its Impact on the Prognosis.Frontiers in oncology · 2021Article
- Interleukin (IL)-7 Signaling in the Tumor Microenvironment.Advances in experimental medicine and biology · 2021Article
Corrections and comments
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Authors and funding
16 authors at 3 institutions in 1 country.
Funding
Abstract
Protracted inhibition of osteoblast (OB) differentiation characterizes multiple myeloma (MM) bone disease and persists even when patients are in long-term remission. However, the underlying pathophysiology for this prolonged OB suppression is unknown. Therefore, we developed a mouse MM model in which the bone marrow stromal cells (BMSCs) remained unresponsive to OB differentiation signals after removal of MM cells. We found that BMSCs from both MM-bearing mice and MM patients had increased levels of the transcriptional repressor Gfi1 compared with controls and that Gfi1 was a novel transcriptional repressor of the critical OB transcription factor Runx2. Trichostatin-A blocked the effects of Gfi1, suggesting that it induces epigenetic changes in the Runx2 promoter. MM-BMSC cell-cell contact was not required for MM cells to increase Gfi1 and repress Runx2 levels in MC-4 before OBs or naive primary BMSCs, and Gfi1 induction was blocked by anti-TNF-α and anti-IL-7 antibodies. Importantly, BMSCs isolated from Gfi1(-/-) mice were significantly resistant to MM-induced OB suppression. Strikingly, siRNA knockdown of Gfi1 in BMSCs from MM patients significantly restored expression of Runx2 and OB differentiation markers. Thus, Gfi1 may have an important role in prolonged MM-induced OB suppression and provide a new therapeutic target for MM bone disease.
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Registered trials
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.