ArticleJournal of experimental & clinical cancer research : CR2025
E2F1-autophagy-ALDH1A1 axis enhances self-renewal and drug resistance of lung cancer stem-like cells in a p53-dependent manner.
Article in Journal of experimental & clinical cancer research : CR, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Frequency-Domain Transformation of cfDNA End-Motif Profiles Enhances Robust Cancer Detection.Genes · 2026Article
- KRT15 identified by scRNA-Seq and machine learning as stemness regulator and prognostic biomarker in ESCC.iScience · 2026Article
- Diagnostic value of peripheral blood leukocyte parameters, NE-WX, LY-Y, MO-WY, MO-Y, MO-Z, and NE-SFL, in lung cancer.Frontiers in oncology · 2026Article
- Construction of a novel risk model for esophageal squamous cell carcinoma associated with purinergic signaling pathways and chemoradiotherapy sensitivity genes.Frontiers in medicine · 2026Article
- NCAPD2 promotes the progression of lung adenocarcinoma through an AKT/MDM2/E2F1 positive feedback loop.Cancer biology & therapy · 2025Article
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10 authors.
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Abstract
Lung adenocarcinoma (LUAD) is a predominant subtype of non-small cell lung adenocarcinoma (NSCLC). It is typically asymptomatic and associated with high mortality rates. Despite recent advancements in screening technologies and therapeutic approaches, its pathogenesis still remains elusive. Therefore, it is imperative to explore new diagnostic markers and therapeutic targets for LUAD management. Cancer stem cells (CSCs) have high self-renewal capacity and incur therapeutic resistance, thus, considered as crucial elements in initiating and promoting tumor development. Contextual to this, the present study reveals the role of the transcriptional activator E2F1 in LUAD oncogenesis and its association with various biological characteristics of lung cancer stem cells (LCSCs). Whereby, it may also serve as a crucial factor in regulating autophagy. Autophagy can modulate stemness by either promoting or inhibiting CSCs characteristics. Pertinently, our study integrated bioinformatics, in-vitro and in-vivo experiments to elucidate that E2F1 can induce ALDH1A1 through autophagy, thus promoting self-renewal and drug resistance of LCSCs, as well as tumorigenicity. Mechanistically, "E2F1-autophagy-ALDH1A1" axis enhanced the self-renewal capacity and drug resistance of LCSCs in a p53-dependent manner, highlighting the potential of E2F1 as a promising marker for LUAD.
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