ArticleOncotarget2016
Mechanism of melanoma cells selective apoptosis induced by a photoactive NADPH analogue.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.
- Genetic variants in TKT and DERA in the nicotinamide adenine dinucleotide phosphate pathway predict melanoma survival.European journal of cancer (Oxford, England : 1990) · 2020Pooled it
- Autophagy as a targeted therapeutic approach for skin cancer: Evaluating natural and synthetic molecular interventions.Cancer pathogenesis and therapy · 2024Review
- The role of mitochondria in the resistance of melanoma to PD-1 inhibitors.Journal of translational medicine · 2023Review
- Targeting M2 Macrophages with a Novel NADPH Oxidase Inhibitor.Antioxidants (Basel, Switzerland) · 2023Article
- The Role of Calcium Signaling in Melanoma.International journal of molecular sciences · 2022Review
- Review
- Distinction between 2'- and 3'-Phosphate Isomers of a Fluorescent NADPH Analogue Led to Strong Inhibition of Cancer Cells Migration.Antioxidants (Basel, Switzerland) · 2021Article
- Discovery of a new molecule inducing melanoma cell death: dual AMPK/MELK targeting for novel melanoma therapies.Cell death & disease · 2021Article
- Dysfunctional autophagy induced by the pro-apoptotic natural compound climacostol in tumour cells.Cell death & disease · 2018Article
- E2F1 inhibition mediates cell death of metastatic melanoma.Cell death & disease · 2018Article
Corrections and comments
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Authors and funding
4 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Melanoma is one of the most lethal cancers when it reaches a metastatic stage. Despite the spectacular achievements of targeted therapies (BRAF inhibitors) or immuno-therapies (anti-CTLA4 or anti-PD1), most patients with melanoma will need additional treatments. Here we used a photoactive NADPH analogue called NS1 to induce cell death by inhibition of NADPH oxidases NOX in melanoma cells, including melanoma cells isolated from patients. In contrast, healthy melanocytes growth was unaffected by NS1 treatment.NS1 established an early Endoplasmic Reticulum stress by the early release of calcium mediated by (a) calcium-dependent redox-sensitive ion channel(s). These events initiated autophagy and apoptosis in all tested melanoma cells independently of their mutational status. The autophagy promoted by NS1 was incomplete. The autophagic flux was blocked at late stage events, consistent with the accumulation of p62, and a close localization of LC3 with NS1 associated with NS1 inhibition of NOX1 in autophagosomes. This hypothesis of a specific incomplete autophagy and apoptosis driven by NS1 was comforted by the use of siRNAs and pharmacological inhibitors blocking different processes. This study highlights the potential therapeutic interest of NS1 inducing cell death by triggering a selective ER stress and incomplete autophagy in melanoma cells harbouring wt and BRAF mutation.
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