ArticleJournal of lipid research2013
Sphingomyelin synthase 1 activity is regulated by the BCR-ABL oncogene.
Article in Journal of lipid research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 30 citations in OpenAlex.
- An integrative approach to studying sphingolipid metabolism reveals p53 as a master regulator of the pathway.Journal of lipid research · 2026Article
- Exploring the role of 338 cerebrospinal fluid metabolites in primary brain malignancies risk: a Mendelian randomization study.Discover oncology · 2025Article
- Identification of metabolic biomarkers and therapeutic targets in the thymoma-associated myasthenia gravis treated with methylprednisolone.Discover oncology · 2025Article
- Dysregulation of sphingolipid metabolism contributes to the pathogenesis of chronic myeloid leukemia.Cell death & disease · 2025Article
- Bioactive Lipids as Chronic Myeloid Leukemia's Potential Biomarkers for Disease Progression and Response to Tyrosine Kinase Inhibitors.Frontiers in immunology · 2022Article
- Ceramide Transfer Protein (CERT): An Overlooked Molecular Player in Cancer.International journal of molecular sciences · 2021Review
- Cholesterol and Sphingolipid Enriched Lipid Rafts as Therapeutic Targets in Cancer.International journal of molecular sciences · 2021Review
- Regulation of human sphingomyelin synthase 1 translation through its 5'-untranslated region.FEBS letters · 2020Article
- Ceramide/Sphingomyelin Rheostat Regulated by Sphingomyelin Synthases and Chronic Diseases in Murine Models.Journal of lipid and atherosclerosis · 2020Review
- UDP-glucose ceramide glucosyltransferase activates AKT, promoted proliferation, and doxorubicin resistance in breast cancer cells.Cellular and molecular life sciences : CMLS · 2018Article
- Bcr-Abl regulation of sphingomyelin synthase 1 reveals a novel oncogenic-driven mechanism of protein up-regulation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- Sphingomyelin synthase 2 overexpression promotes cisplatin-induced apoptosis of HepG2 cells.Oncology letters · 2018Article
- Aneuploid Cell Survival Relies upon Sphingolipid Homeostasis.Cancer research · 2017Article
- Runx1 Orchestrates Sphingolipid Metabolism and Glucocorticoid Resistance in Lymphomagenesis.Journal of cellular biochemistry · 2017Article
- Role of Sphingolipids and Metabolizing Enzymes in Hematological Malignancies.Molecules and cells · 2015Review
- Sphingomyelin Synthase 1 Regulates Neuro-2a Cell Proliferation and Cell Cycle Progression Through Modulation of p27 Expression and Akt Signaling.Molecular neurobiology · 2015Article
- Phosphorylation of serine palmitoyltransferase long chain-1 (SPTLC1) on tyrosine 164 inhibits its activity and promotes cell survival.The Journal of biological chemistry · 2013Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
Abstract
Sphingomyelin synthase (SMS) produces sphingomyelin while consuming ceramide (a negative regulator of cell proliferation) and forming diacylglycerol (DAG) (a mitogenic factor). Therefore, enhanced SMS activity could favor cell proliferation. To examine if dysregulated SMS contributes to leukemogenesis, we measured SMS activity in several leukemic cell lines and found that it is highly elevated in K562 chronic myelogenous leukemia (CML) cells. The increased SMS in K562 cells was caused by the presence of Bcr-abl, a hallmark of CML; stable expression of Bcr-abl elevated SMS activity in HL-60 cells while inhibition of the tyrosine kinase activity of Bcr-abl with Imatinib mesylate decreased SMS activity in K562 cells. The increased SMS activity was the result of up-regulation of the Sms1 isoform. Inhibition of SMS activity with D609 (a pharmacological SMS inhibitor) or down-regulation of SMS1 expression by siRNA selectively inhibited the proliferation of Bcr-abl-positive cells. The inhibition was associated with an increased production of ceramide and a decreased production of DAG, conditions that antagonize cell proliferation. A similar change in lipid profile was also observed upon pharmacological inhibition of Bcr-abl (K526 cells) and siRNA-mediated down-regulation of BCR-ABL (HL-60/Bcr-abl cells). These findings indicate that Sms1 is a downstream target of Bcr-abl, involved in sustaining cell proliferation of Bcr-abl-positive cells.
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Registered trials
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