ArticleCancer research communications2026
m6A Modification of ATOX1 Inhibits Acute Myeloid Leukemia Progression by Promoting Cuproptosis.
Article in Cancer research communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Epigenetic regulation of cuproptosis in cancer: mechanisms, microenvironment, and therapeutic implications.Frontiers in cell and developmental biology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cuproptosis, a regulated cell death caused by copper-dependent enzyme overactivation in the tricarboxylic acid cycle, leads to proteotoxic stress. Although the copper chaperone human antioxidant protein 1 (ATOX1) plays a key role in cuproptosis, its link to acute myeloid leukemia (AML) progression remains unclear. In this study, elesclomol (ES) or disulfiram (DSF)/Cu was used to induce cuproptosis, and bathocuproine disulfonic acid (BCS) was used to inhibit it. An AML xenograft mouse model was also established to validate their effects in tumor tissue. Our study demonstrated that ATOX1 is downregulated in AML. Knockdown of ATOX1 promoted cell viability and proliferation, reduced the proportion of cells in the G2-M phase, and decreased cell death. In contrast, overexpression of ATOX1 produced the opposite outcomes. Moreover, ATOX1 knockdown attenuated ES-/Cu-induced cuproptosis in AML cells, whereas ATOX1 overexpression enhanced it. This promoting effect of ATOX1 overexpression was effectively counteracted by the copper chelator BCS. Delving deeper, we discovered that ATOX1 is subject to N6-methyladenosine (m6A) modification mediated by AlkB homolog 5 (ALKBH5). Consequently, ALKBH5 can influence cuproptosis in AML cells by regulating ATOX1 expression. In vivo, the role of the ALKBH5-ATOX1 axis in AML progression has also been confirmed. In conclusion, the demethylase ALKBH5 downregulates ATOX1 by reducing its m6A levels, thereby modulating cuproptosis in AML-a mechanism that offers potential novel insights and therapeutic targets for AML treatment. SIGNIFICANCE: This study reveals that in AML, the demethylase ALKBH5 downregulates ATOX1 expression by reducing its m6A modification, thereby inhibiting cuproptosis and promoting AML progression. This mechanism provides a novel potential therapeutic target.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.