ArticleMolecules (Basel, Switzerland)2017
Exploring the Antitumor Mechanism of High-Dose Cytarabine through the Metabolic Perturbations of Ribonucleotide and Deoxyribonucleotide in Human Promyelocytic Leukemia HL-60 Cells.
Article in Molecules (Basel, Switzerland), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 31 citations in OpenAlex.
- Rapid Transcription Dynamics Confers Cytarabine Resistance in Acute Myeloid Leukemia.Blood cancer discovery · 2026Article
- 3'-RSC chemical biology · 2025Article
- Platelet-derived microparticles enhance Ara-C-induced cell death in acute lymphoblastic leukemia (Nalm-6).BioImpacts : BI · 2025Article
- FT538, iPSC-derived NK cells, enhance AML cell killing when combined with chemotherapy.Journal of cellular and molecular medicine · 2025Article
- CSE1L Silencing Enhances Cytarabine-mediated Cytotoxicity in Acute Myeloid Leukemia.Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion · 2024Article
- Prediction of miRNA‑mRNA network regulating the migration ability of cytarabine‑resistant HL60 cells.Biomedical reports · 2024Article
- Magnetosomes as Potential Nanocarriers for Cancer Treatment.Current drug delivery · 2024Review
- EIF4A inhibition targets bioenergetic homeostasis in AML MOLM-14 cells in vitro and in vivo and synergizes with cytarabine and venetoclax.Journal of experimental & clinical cancer research : CR · 2022Article
- Review
- Proteasome Inhibitors Interrupt the Activation of Non-Canonical NF-κB Signaling Pathway and Induce Cell Apoptosis in Cytarabine-Resistant HL60 Cells.International journal of molecular sciences · 2021Article
- Narrative review of targetable features of pediatric acute myeloid leukemia from molecular and metabolic perspectives.Pediatric medicine (Hong Kong, China) · 2021Article
- Article
- A comprehensive review of genetic alterations and molecular targeted therapies for the implementation of personalized medicine in acute myeloid leukemia.Journal of molecular medicine (Berlin, Germany) · 2020Review
- Review
- Improving the Clinical Application of Natural Killer Cells by Modulating Signals Signal from Target Cells.International journal of molecular sciences · 2019Article
- Impact of diverse chemotherapeutic agents and external factors on activation of brown adipose tissue in a large patient collective.Scientific reports · 2019Article
- Mathematical models for cytarabine-derived myelosuppression in acute myeloid leukaemia.PloS one · 2019Article
- Oral cytarabine ocfosfate pharmacokinetics and assessment of leukocyte biomarkers in normal dogs.Journal of veterinary internal medicineArticle
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Authors and funding
7 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Despite the apparent clinical benefits of high-dose cytarabine (Ara-C) over lower dose Ara-C in acute myeloid leukemia (AML) therapy, the mechanism behind high-dose Ara-C therapy remains uncertain. In this study, a LC-MS-based method was carried out to investigate the metabolic alteration of ribonucleotide and deoxyribonucleotide in human promyelocytic leukemia cells (HL-60) after treatment with Ara-C to reveal its antitumor mechanism. The metabolic results revealed that four nucleotides (ATP, ADP, CDP, and dCTP) could be used as potential biomarkers indicating the benefit of high-dose Ara-C over lower dose Ara-C treatment. Combining metabolic perturbation and cell cycle analysis, we conjectured that, apart from the acknowledged mechanism of Ara-C on tumor inhibition, high-dose Ara-C could present a specific action pathway. It was suggested that the pronounced rise in AMP/ATP ratio induced by high-dose Ara-C can trigger AMP-activated protein kinase (AMPK) and subsequently Forkhead Box, class O (FoxO), to promote cell cycle arrest. Moreover, the significant decrease in CDP pool induced by high-dose Ara-C might further accelerate the reduction of dCTP, which then aggravates DNA synthesis disturbance. As a result, all of these alterations led to heightened tumor inhibition. This study provides new insight in the investigation of potential mechanisms in the clinical benefits of high-dose Ara-C in therapy for AML.
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