ArticleTranslational cancer research2019
Melatonin enhances arsenic trioxide-induced cytotoxicity by modulating autophagy in an acute promyelocytic leukemia cell line.
Article in Translational cancer research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed, 8 citations in OpenAlex.
- Melatonin combined with antineoplastic drugs or natural products for cancer treatment: An update.Current research in pharmacology and drug discovery · 2025Review
- Melatonin as a regulator of apoptosis in leukaemia: molecular mechanism and therapeutic perspectives.Frontiers in pharmacology · 2023Review
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9 authors at 1 institution in 1 country.
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Abstract
backgroundArsenic trioxide (ATO)-containing therapeutic strategies are widely used in the treatment of acute promyelocytic leukemia (APL). Growing evidence has shown that melatonin enhances the radio- or chemo-sensitivity of numerous cancer cells. However, whether melatonin is capable of enhancing the cytotoxic effects of ATO in APL cells remains unknown.
methodsThe present study conducted a 24 h melatonin exposure followed by additional 12, 24 or 48 h ATO exposure in the APL cell line NB4 with or without autophagy-related protein 7 (ATG7) silencing by RNA interference. Cell cytotoxicity was evaluated by Cell Counting Kit-8 (CCK-8) and lactate dehydrogenase (LDH) assays. Cell apoptosis was assessed by Annexin-V/propidium iodide assay and western blotting against cleaved caspase 3, Bax and Bcl-2. Autophagy was evaluated by western blotting against LC3.
resultsPre-treatment with a non-cytotoxic dose of melatonin significantly enhanced ATO-mediated reduced cell viability and increased LDH release. Furthermore, melatonin pre-treatment also enhanced ATO-mediated increase in early and late apoptosis, as well as the expression of Bax and cleaved caspase 3, while further decreasing ATO-mediated reduced expression of Bcl-2. Concomitantly, melatonin pre-treatment increased LC3II expression and enhanced the ATO-mediated elevation in LC3II expression. However, autophagy inhibition by ATG7 silencing blocked the enhancing effects of melatonin on ATO-induced apoptosis and cytotoxicity. These findings indicated that melatonin pre-treatment enhances ATO-induced cytotoxicity by modulating ATG7-mediated autophagy.
conclusionsMelatonin could represent a valuable adjuvant to ATO in APL treatment, particularly in patients with ATO-resistant APL.
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