ArticleDaru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences2024
Chidamide inhibits cell glycolysis in acute myeloid leukemia by decreasing N6-methyladenosine-related GNAS-AS1.
Article in Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- mFrontiers in cell and developmental biology · 2026Review
- Uncomplexed-TSC1 deploys novel mTORC1-independent pathway to exacerbate the liver glycogen storage in TSC.Cell death & disease · 2025Article
- ZFAS1/STAT3 axis modulates imatinib resistance of chronic myeloid leukemia cells through glucose metabolism reprogramming.Frontiers in oncology · 2025Article
- Histone deacetylase inhibitors for leukemia treatment: current status and future directions.European journal of medical research · 2024Review
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6 authors.
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Abstract
backgroundAcute myeloid leukemia (AML) is a hematopoietic malignancy. Chidamide has shown anti-cancer effect in different malignancies. The function of Chidamide in glycolysis in AML cells remains unclear.
methodsAML cells were treated with 1000 nM Chidamide for 48 h. The levels of long non-coding RNA-GNAS-AS1, miR-34a-5p, glycolysis-related proteins, and Ras homolog gene family (RhoA)/Rho-associated protein kinase (ROCK) signaling-related proteins were detected by qRT-PCR or western blot. Cell viability and apoptosis were measured by CCK-8 and flow cytometry. Glycolysis levels were measured by assay kits. GNAS-AS1 N6-methyladenosine (m6A) modification level was detected by methylated RNA immunoprecipitation sequencing. The combined targets of miR-34a-5p were validated using a dual-luciferase reporter assay. BALB/C nude mice were selected for subcutaneous tumor validation. Chidamide at a dosage of 25 mg/kg was used in the animal study.
resultsGNAS-AS1 promoted glycolysis in AML cells by upregulating the expression of glycolysis-related proteins and increasing glucose consumption, lactate production, ATP generation, and the extracellular acidification rate. Chidamide treatment suppressed WT1-associated protein (WTAP)-mediated RNA m6A modification of GNAS-AS1. Chidamide downregulated GNAS-AS1 to inhibit glycolysis in AML cells. GNAS-AS1 targeted miR-34a-5p to promote insulin-like growth factor 2 mRNA-binding protein (IGF2BP2) expression. IGF2BP2 inhibition reversed the promoting effect of miR-34a-5p knockdown on glycolysis and RhoA/ROCK pathway in Chidamide-treated cells. GNAS-AS1 overexpression abolished the inhibitory effect of Chidamide on AML tumorigenesis in vivo by modulating the RhoA/ROCK pathway.
conclusionChidamide inhibited glycolysis in AML by repressing WTAP-mediated GNAS-AS1 m6A modification and then regulating the miR-34a-5p/IGF2BP2 axis.
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