ArticleOncology letters2022
Potential of a sphingosine 1-phosphate receptor antagonist and sphingosine kinase inhibitors as targets for multiple myeloma treatment.
Article in Oncology letters, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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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.
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Who cites it
7 citing papers in PubMed, 7 citations in OpenAlex.
- Therapeutic potential of the sphingosine kinase 2 inhibitor opaganib.Pharmaceutical science advances · 2026Review
- Immunosuppressive Effects of Multiple Myeloma-Derived Extracellular Vesicles Through T Cell Exhaustion.Cancer science · 2025Article
- Dissecting the Puzzling Roles of FAM46C: A Multifaceted Pan-Cancer Tumour Suppressor with Increasing Clinical Relevance.Cancers · 2024Review
- The emerging roles of sphingosine 1-phosphate and SphK1 in cancer resistance: a promising therapeutic target.Cancer cell international · 2024Review
- Lipid metabolic vulnerabilities of multiple myeloma.Clinical and experimental medicine · 2023Review
- Obesity and myeloma: Clinical and mechanistic contributions to disease progression.Frontiers in endocrinology · 2023Review
- Role of Sphingolipids in Multiple Myeloma Progression, Drug Resistance, and Their Potential as Therapeutic Targets.Frontiers in oncology · 2022Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sphingosine 1-phosphate (S1P) is a bioactive lipid involved in cancer progression through its binding to S1P receptors (S1PRs). However, the association between multiple myeloma (MM) and S1P is unclear. The current study aimed to investigate the potential anti-cancer effects of fingolimod and sphingosine kinase (SK) inhibitors in myeloma cells and the effects of S1P-induced chemoresistance and neovascularization on MM cell proliferation. MM cell lines were treated with the S1PR1 antagonist fingolimod and the SK inhibitors ABC294640 and SK1-I, after which cell proliferation was measured. Protein expression was also assessed under each condition using immunoblotting. Serum S1P levels in patients with MM, monoclonal gammopathy of undetermined significance and healthy volunteers were assessed. Human umbilical vessel cells (HUVECs) were co-cultured with anti-S1P agents to assess the effect on cell migration. All treatments suppressed myeloma cell proliferation and caspase-3-mediated apoptosis by suppressing S1P activity. These findings suggest that S1P activation is associated with proliferation and survival for MM cells. S1P attenuated the proteosome inhibitor (PI) effect, while the anti-S1P agents recovered the effect. In addition, S1P promoted the migration and proliferation of HUVECs, whereas the S1P inhibitors reduced the influence of S1P. This study highlights the therapeutic potential of anti-S1P agents for MM treatment. Inhibition of S1P function may overcome resistance to PI developed by myeloma cells and inhibit the changes to the bone marrow microenvironment via neovascularization.
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