ArticleCell death discovery2022
Down-regulated m6A reader FTO destabilizes PHF1 that triggers enhanced stemness capacity and tumor progression in lung adenocarcinoma.
Article in Cell death discovery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 34 citations in OpenAlex.
- The AHCY-adenosine complex rewires mRNA methylation to enhance fatty acid biosynthesis and tumorigenesis.Cell research · 2026Article
- The role of m6A modification in non-small cell lung cancer: functional insights and impact on therapy resistance.Cancer cell international · 2025Review
- Advances in research on RNA methylation and cancer radiotherapy resistance.Frontiers in oncology · 2025Review
- m6A-Mediated Stabilization of PRMT9 mRNA by IGF2BP1 Drives Proliferation and Metastasis in Lung Adenocarcinoma.Analytical cellular pathology (Amsterdam) · 2025Article
- A novel nomogram model for lung adenocarcinoma subtypes based on RNA-modification regulatory genes.Heliyon · 2024Article
- mAmerican journal of cancer research · 2024Article
- Siglec 15 as a biomarker or a druggable molecule for non-small cell lung cancer.Journal of cancer research and clinical oncology · 2023Review
- FTO facilitates cancer metastasis by modifying the mCell communication and signaling : CCS · 2023Article
- METTL3 exerts synergistic effects on m6A methylation and histone modification to regulate the function of VGF in lung adenocarcinoma.Clinical epigenetics · 2023Article
- The critical roles of m6A RNA methylation in lung cancer: from mechanism to prognosis and therapy.British journal of cancer · 2023Review
- Review
- The role of m6A demethylases in lung cancer: diagnostic and therapeutic implications.Frontiers in immunology · 2023Review
- Construction of a ferroptosis scoring system and identification of LINC01572 as a novel ferroptosis suppressor in lung adenocarcinoma.Frontiers in pharmacology · 2022Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aberrant epigenetic drivers or suppressors contribute to LUAD progression and drug resistance, including KRAS, PTEN, Keap1. Human Plant Homeodomain (PHD) finger protein 1 (PHF1) coordinates with H3K36me3 to increase nucleosomal DNA accessibility. Previous studies revealed that PHF1 is markedly upregulated in various tumors and enhances cell proliferation, migration and tumorigenesis. However, its roles in LUAD are still unknown. We aimed to depict the biological roles of PHF1 and identify useful targets for clinical treatment of LUAD. Based on the bioinformatic analysis, we found that PHF1 was down-regulated in LUAD samples and low PHF1 expressions correlated with unfavorable clinical characteristics. Patients with low PHF1 had poorer survival outcomes relative to those with high PHF1. Targeting PHF1 potentiated cell growth, migration and in vivo proliferation. Mechanistically, FTO mediated the stabilization of PHF1 mRNA by demethylating m6A, which particularly prevented YTHDF2 from degrading PHF1 transcripts. Of note, FTO also expressed lowly in LUAD that predicts poor prognosis of patients. FTO inhibition promoted LUAD progression, and PHF1 overexpression could reverse the effect. Lastly, down-regulated FTO/PHF1 axis could mainly elevate FOXM1 expression to potentiate the self-renewal capacity. Targeting FOXM1 was effective to suppress PHF1
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Registered trials
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