ArticleAmerican journal of cancer research2025
Role and mechanism of the CBX4-HDAC5-CERS6 axis in disrupting sphingomyelin metabolism in acute myeloid leukemia.
Article in American journal of cancer research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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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Who cites it
1 citing paper in PubMed.
- From transcriptomic profiling to precision oncology: a bibliometric analysis of RNA sequencing in acute myeloid leukemia.Frontiers in medicine · 2026Article
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Authors and funding
7 authors.
Funding
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Abstract
objectiveTo investigate the mechanism by which the CBX4-HDAC5-CERS6 axis regulates sphingolipid metabolism in acute myeloid leukemia (AML), with the goal of providing new theoretical foundations for the targeted therapy of AML.
methodsThis prospective study involved 50 AML patients and 50 healthy controls. The expression levels of CBX4, CERS6, and free ceramide were detected. RNA sequencing, proteomics, and lipidomics were employed to analyze CBX4's regulatory effects on sphingolipid metabolism-related genes and pathways. Using THP-1 and KG-1 cell lines, we validated the molecular mechanisms of the CBX4-HDAC5-CERS6 axis through techniques including gene knockdown (siRNA), overexpression, chromatin immunoprecipitation (ChIP), and dual-luciferase reporter assays. CCK-8 assay, flow cytometry, and Western blot were used to analyze the effects of CBX4 on cell proliferation, cell cycle, and key signaling pathways.
resultsCBX4 was significantly overexpressed in AML cells, with its expression levels markedly higher in THP-1 and KG-1 cell lines compared with CD34
conclusionThe CBX4-HDAC5-CERS6 axis influences AML malignant progression by regulating sphingolipid metabolism, and targeted intervention of this axis may represent a novel therapeutic strategy for AML.
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