ArticleCell death & disease2025
The RNA-binding protein CELF1 targets ATG5 to regulate autophagy and promote drug resistance in acute myeloid leukemia.
Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.
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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
4 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Non-coding RNAs' pivotal importance in modulation of cancer sensitivity to Topotecan: a systematic review.Medical oncology (Northwood, London, England) · 2025Pooled it
- Mechanistic insights and clinical implications of RNA-binding proteins in prostate cancer.Discover oncology · 2026Review
- Targeting autophagy in dysfunctional tumor vasculature.iScience · 2025Review
- Targeting cell death pathways in acute myeloid leukemia: Molecular mechanisms and clinical implications (Review).Oncology reports · 2025Review
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Authors and funding
8 authors.
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Abstract
Acute myeloid leukemia (AML) is a blood cancer characterized by uncontrolled growth of myeloid cells. Overcoming AML treatment resistance, particularly to anthracycline-based drugs like doxorubicin (ADR), poses a challenge. This study investigated the role of CELF1, an RNA-binding protein, in ADR resistance and autophagy regulation in AML. CELF1 expression was elevated in multiple tumor types, including AML. AML cell lines exhibit varying levels of CELF1 expression, with drug-resistant cell lines showing higher CELF1 expression compared to parental cells. CELF1 knockdown reduced drug resistance, promoted cell death, and inhibited autophagy. Mechanistic analysis identified ATG5 as a potential CELF1-regulated target gene, with CELF1 knockdown reducing ATG5 expression and mRNA decay. These findings indicate that targeting CELF1 could overcome ADR resistance in AML by modulating autophagy through ATG5 regulation, highlighting its clinical significance as a therapeutic target for enhancing ADR response in AML.
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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.