ArticleCell biochemistry and biophysics2025
METTL3/YTDHF1 Stabilizes CSRP1 mRNA to Regulate Glycolysis and Promote Acute Myeloid Leukemia Progression.
Article in Cell biochemistry and biophysics, 2025. 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.
- METTL3-YTHDF1-driven mMolecular and cellular biochemistry · 2026Article
- RNA Regulatory Networks: Key Hubs in the Panorama of Cancer and Emerging Therapeutic Targets.MedComm · 2026Review
- The role of m6A RNA methyltransferase METTL3 in drug resistance mechanisms in acute myeloid leukemia.Blood research · 2026Review
- Decoding mFrontiers in immunology · 2025Review
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Authors and funding
5 authors.
Funding
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Abstract
CSRP1 (Cysteine and Glycine-Rich Protein 1) is a protein often overactivated in various cancers, promoting cell proliferation and survival, making it a key factor in cancer development. However, it is worth noting that the effect of this protein on the glycolysis process in Acute Myeloid Leukemia (AML) has not yet been studied. This study aims to investigate the role of the METTL3/YTHDF1 axis in regulating Glycolysis and its impact on AML progression by stabilizing CSRP1 mRNA. We analyzed CSRP1 expression in AML tissues and cell lines using quantitative real-time PCR (qRT-PCR) and Western blotting. Functional assays, including cell viability, colony formation, glycolysis related indicators, were performed to assess the impact of CSRP1 knockdown or overexpression on AML cells. RNA immunoprecipitation (RIP) and RNA stability assays were conducted to elucidate the mechanism of METTL3/YTHDF1-mediated regulation of CSRP1 mRNA. CSRP1 was significantly upregulated in AML tissues and cell lines. Knockdown of CSRP1 inhibited AML cell proliferation and glycolysis. Overexpression of CSRP1 promoted AML cell survival. Mechanistically, METTL3 enhanced CSRP1 mRNA stability via m6A modification, recognized and bound by YTHDF1, preventing mRNA degradation. The METTL3/YTHDF1/ CSRP1 axis plays a critical role in AML progression by regulating glycolysis. Targeting this pathway may provide a novel therapeutic strategy for AML treatment.
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