ArticleOncology letters2021
Sphingosine kinases are involved in the regulation of all-trans retinoic acid sensitivity of K562 chronic myeloid leukemia cells.
Article in Oncology letters, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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.
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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
8 citing papers in PubMed, 13 citations in OpenAlex.
- Article
- Role of Sphingosine-1-Phosphate Signaling Pathway in Pancreatic Diseases.International journal of molecular sciences · 2024Review
- Systems Biology for Drug Target Discovery in Acute Myeloid Leukemia.International journal of molecular sciences · 2024Article
- Integrative roles of sphingosine kinase in liver pathophysiology.Toxicological research · 2023Review
- Discovery and design of dual inhibitors targeting Sphk1 and Sirt1.Journal of molecular modeling · 2023Article
- Endoplasmic Reticulum Stress and Mitochondrial Stress in Drug-Induced Liver Injury.Molecules (Basel, Switzerland) · 2023Review
- The Role of Sphingolipids Metabolism in Cancer Drug Resistance.Frontiers in oncology · 2021Review
- Therapeutic Potential of SphK1 Inhibitors Based on Abnormal Expression of SphK1 in Inflammatory Immune Related-Diseases.Frontiers in pharmacology · 2021Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The efficacy of all-trans retinoic acid (ATRA) for the treatment of chronic myeloid leukemia (CML) has been reported to be limited both as single-drug treatment or in combination with other drugs. Our previous study demonstrated that sphingosine 1-phosphate attenuated the effects of ATRA on human colon cancer cells by blocking the expression of retinoic acid receptor β. The aim of the present study was to investigate whether the ATRA-dependent proliferation inhibition of K562 cells was regulated by sphingosine kinases (SphKs). The results of cell proliferation assay and reverse transcription-PCR demonstrated that ATRA may exert synergistic effects with the SphK1 inhibitor SKI 5C or the pan-SphK inhibitor SKI II to inhibit the proliferation of K562 cells and upregulate the expression levels of the ATRA-inducible enzyme cytochrome P450 26A1 (CYP26A1). Knocking down the expression of SphK1 or SphK2 in K562 cells by small interfering RNA enhanced the inhibitory effects of ATRA and induced the expression of CYP26A1. Crude asterosaponins, which abrogated the expression of SphK2, also enhanced the effects of ATRA on K562 cells. In conclusion, the results of the present study demonstrated that SphKs may be involved in the regulation of the sensitivity of CML cells to ATRA.
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