ArticleOncotarget2014
Notch signaling drives multiple myeloma induced osteoclastogenesis.
Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
30 citing papers in PubMed, 48 citations in OpenAlex.
- Jagged-dependent Notch signaling governs extracellular vesicle bioactivity in multiple myeloma.Leukemia · 2026Article
- Review
- Communication between bone marrow mesenchymal stem cells and multiple myeloma cells: Impact on disease progression.World journal of stem cells · 2023Review
- Tumor Microenvironment, Clinical Features, and Advances in Therapy for Bone Metastasis in Gastric Cancer.Cancers · 2022Review
- Extracellular vesicles mediate the communication between multiple myeloma and bone marrow microenvironment in a NOTCH dependent way.Haematologica · 2022Article
- Targeting Notch Inhibitors to the Myeloma Bone Marrow Niche Decreases Tumor Growth and Bone Destruction without Gut Toxicity.Cancer research · 2021Article
- Morphogens and growth factor signalling in the myeloma bone-lining niche.Cellular and molecular life sciences : CMLS · 2021Review
- The multifunctional role of Notch signaling in multiple myeloma.Journal of cancer metastasis and treatment · 2021Article
- Restoring Tissue Homeostasis at Metastatic Sites: A Focus on Extracellular Vesicles in Bone Metastasis.Frontiers in oncology · 2021Review
- Article
- A Gli inhibitor GANT61 suppresses cell proliferation, promotes cell apoptosis and induces G1/G0 cycle retardation with a dose- and time-dependent manner through inhibiting Notch pathway in multiple myeloma.Cell cycle (Georgetown, Tex.) · 2020Article
- Multiple myeloma exploits Jagged1 and Jagged2 to promote intrinsic and bone marrow-dependent drug resistance.Haematologica · 2020Article
- Osteocytes and Bone Metastasis.Frontiers in endocrinology · 2020Review
- Multiple Myeloma Cells Alter Adipogenesis, Increase Senescence-Related and Inflammatory Gene Transcript Expression, and Alter Metabolism in Preadipocytes.Frontiers in oncology · 2020Article
- Extracellular Vesicles Enhance Multiple Myeloma Metastatic Dissemination.International journal of molecular sciences · 2019Review
- The role of oncogenic Notch2 signaling in cancer: a novel therapeutic target.American journal of cancer research · 2019Review
- Re-establishing Apoptosis Competence in Bone Associated Cancers via Communicative Reprogramming Induced Through Notch Signaling Inhibition.Frontiers in pharmacology · 2019Review
- Myeloma Bone Disease: Update on Pathogenesis and Novel Treatment Strategies.Pharmaceutics · 2018Review
- V-ATPases and osteoclasts: ambiguous future of V-ATPases inhibitors in osteoporosis.Theranostics · 2018Review
- Cancer Cells Exploit Notch Signaling to Redefine a Supportive Cytokine Milieu.Frontiers in immunology · 2018Review
Corrections and comments
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Authors and funding
15 authors at 6 institutions in 3 countries.
Funding
Abstract
Multiple myeloma (MM) is closely associated with bone destruction. Once migrated to the bone marrow, MM cells unbalance bone formation and resorption via the recruitment and maturation of osteoclast precursors. The Notch pathway plays a key role in different types of cancer and drives several biological processes relevant in MM, including cell localization within the bone marrow, proliferation, survival and pharmacological resistance. Here we present evidences that MM can efficiently drive osteoclastogenesis by contemporaneously activating Notch signaling on tumor cells and osteoclasts through the aberrant expression of Notch ligands belonging to the Jagged family. Active Notch signaling in MM cells induces the secretion of the key osteoclastogenic factor, RANKL, which can be boosted in the presence of stromal cells. In turn, MM cells-derived RANKL causes the upregulation of its receptor, RANK, and Notch2 in pre-osteoclasts. Notch2 stimulates osteoclast differentiation by promoting autocrine RANKL signaling. Finally, MM cells through Jagged ligands expression can also activate Notch signaling in pre-osteoclast by direct contact. Such synergism between tumor cells and pre-osteoclasts in MM-induced osteoclastogenesis can be disrupted by silencing tumor-derived Jagged1 and 2. These results make the Jagged ligands new promising therapeutic targets in MM to contrast bone disease and the associated co-morbidities.
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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.