ArticleInternational journal of molecular sciences2015
Gentamicin arrests cancer cell growth: the intriguing involvement of nuclear sphingomyelin metabolism.
Article in International journal of molecular sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 27 citations in OpenAlex.
- Sphingomyelin regulates the transcriptional machinery in nuclear lipid microdomains.Communications biology · 2025Article
- Machine Learning-Based Prognostic Signature in Breast Cancer: Regulatory T Cells, Stemness, and Deep Learning for Synergistic Drug Discovery.International journal of molecular sciences · 2025Article
- Unraveling the Anti-Cancer Mechanisms of Antibiotics: Current Insights, Controversies, and Future Perspectives.Antibiotics (Basel, Switzerland) · 2024Review
- A rapid screening platform to coculture bacteria within tumor spheroids.Nature protocols · 2022Review
- Cell surface sphingomyelin: key role in cancer initiation, progression, and immune evasion.Lipids in health and disease · 2021Review
- Cholesterol and Sphingolipid Enriched Lipid Rafts as Therapeutic Targets in Cancer.International journal of molecular sciences · 2021Review
- Gentamicin Targets Acid Sphingomyelinase in Cancer: The Case of the Human Gastric Cancer NCI-N87 Cells.International journal of molecular sciences · 2019Article
- A Role for Neutral Sphingomyelinase in Wound Healing Induced by Keratinocyte Proliferation upon 1International journal of molecular sciences · 2019Article
- Niemann-Pick Type A Disease: Behavior of Neutral Sphingomyelinase and Vitamin D Receptor.International journal of molecular sciences · 2019Article
- Nuclear lipid mediators: Role of nuclear sphingolipids and sphingosine-1-phosphate signaling in epigenetic regulation of inflammation and gene expression.Journal of cellular biochemistry · 2018Review
- Effect of Vitamin D in HN9.10e Embryonic Hippocampal Cells and in Hippocampus from MPTP-Induced Parkinson's Disease Mouse Model.Frontiers in cellular neuroscience · 2018Article
- Acid sphingomyelinase as target of Lycium Chinense: promising new action for cell health.Lipids in health and disease · 2016Article
- Why high cholesterol levels help hematological malignancies: role of nuclear lipid microdomains.Lipids in health and disease · 2016Article
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Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The use of gentamicin for the treatment of bacterial infection has always been an interesting and highly speculated issue for the scientific community. Conversely, its effect on cancer cells has been very little investigated. We studied the effect of high doses of gentamicin on non-Hodgkin's T-cell human lymphoblastic lymphoma (SUP-T1). We showed that gentamicin delayed cell growth and induced cell death in lymphoma cells with a rather mild effect on lymphocytes. In SUP-T1 cells, GAPDH, B2M, CDKN1A and CDKN1B were down-expressed in comparison with lymphocytes. Gentamicin treatment in SUP-T1 cells restored the expression of GAPDH, B2M and CDKN1A to values similar to those of lymphocytes and caused overexpression of CDKN1B. The drug acted via sphingomyelin metabolism; in whole cells, sphingomyelinase activity was stimulated, whereas in purified nuclei, sphingomyelinase activity was inhibited and that of sphingomyelin-synthase was stimulated, with a consequent high level of nuclear sphingomyelin content. We suggest that the increase of nuclear sphingomyelin might enrich the nucleus of lipid microdomains that act as a platform for active chromatin and, thus, might be responsible for gene expression. It is possible that in lymphoblastic lymphoma, high doses of gentamicin induce a beneficial therapeutic outcome.
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