ArticleCell death & disease2020
Exosome-transmitted lncRNA UFC1 promotes non-small-cell lung cancer progression by EZH2-mediated epigenetic silencing of PTEN expression.
Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 papers, 4 of them syntheses that pooled it.
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Who cites it
114 citing papers in PubMed, 4 syntheses or guidelines pooled it, 204 citations in OpenAlex.
- Diagnostic Accuracy of Exosomal Long Noncoding RNAs in Diagnosis of NSCLC: A Meta-Analysis.Molecular diagnosis & therapy · 2024Pooled it
- Diagnostic value of exosomal noncoding RNA in lung cancer: a meta-analysis.Frontiers in oncology · 2024Pooled it
- Unveiling the functional paradigm of exosome-derived long non-coding RNAs (lncRNAs) in cancer: based on a narrative review and systematic review.Journal of cancer research and clinical oncology · 2023Pooled it
- Pooled it
- In Vivo Direct Reprogramming: Current Progress and Future Prospects from Mechanisms to Therapeutic Application.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Narrative review-the emerging role, functions, and mechanisms of UFMylation in cancers.Translational cancer research · 2026Review
- Review
- Early-stage multi-cancer detection through a plasma extracellular vesicle protein signature.Cell reports. Medicine · 2026Article
- Research progress on long non‑coding RNAs in lung cancer (Review).Molecular medicine reports · 2026Review
- Novel lncRNA Signature (UFC1/PTENP1) as a Molecular Biomarker for the Diagnosis and Prognosis of Hepatocellular Carcinoma in an Egyptian Cohort.Current issues in molecular biology · 2026Article
- The UFM1 Conjugation System: A Master Regulator of Cellular Stress Surveillance in Human Disease.Biology · 2026Review
- Extracellular vesicles derived from irradiated tumor cells foster immunosuppressive macrophages formation to promote esophageal squamous cell carcinoma immune evasion.International journal of biological sciences · 2026Article
- Deciphering the enigma: long noncoding RNAs in disease pathogenesis and therapeutic prospects.Molecular and cellular biochemistry · 2025Review
- Long non-coding RNAs and signaling networks in non-small cell lung cancer: mechanistic insights into tumor pathogenesis.Cancer gene therapy · 2025Review
- Significance of Epigenetic Alteration in Cancer-Associated Fibroblasts on the Development of Carcinoma.International journal of molecular sciences · 2025Review
- Exosomal long non-coding RNAs in gastrointestinal cancer: chemoresistance mediators and therapeutic targets.Journal of translational medicine · 2025Review
- The role of long non-coding RNAs in lung cancer metastasis: Molecular mechanisms, pathogenesis and clinical implications.Clinical and translational medicine · 2025Review
- Intratumoral heterogeneity and drug resistance in cancer.Cancer cell international · 2025Review
- Exosomal RNAs and EZH2: unraveling the molecular dialogue driving tumor progression.Medical oncology (Northwood, London, England) · 2025Review
- The role of tumor-derived exosomal LncRNA in tumor metastasis.Cancer gene therapy · 2025Review
54 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Long non-coding RNAs (LncRNAs) have been suggested as important regulators of cancer development and progression in non-small cell lung cancer (NSCLC). Nevertheless, the biological roles and clinical significance of lncRNA UFC1 in NSCLC remain unclear. We detected the expression of UFC1 in tumor tissues, serum, and serum exosomes of NSCLC patients by qRT-PCR. Gene overexpression or silencing were used to examine the biological roles of UFC1 in NSCLC. RNA immunoprecipitation and ChIP assays were performed to evaluate the interaction between UFC1 and enhancer of zeste homolog 2 (EZH2) and the binding of EZH2 to PTEN gene promoter. Rescue study was used to access the importance of PTEN regulation by UFC1 in NSCLC progression. UFC1 expression was upregulated in tumor tissues, serum, and serum exosomes of NSCLC patients and high level of UFC1 was associated with tumor infiltration. UFC1 knockdown inhibited NSCLC cell proliferation, migration and invasion while promoted cell cycle arrest and apoptosis. UFC1 overexpression led to the opposite effects. Mechanistically, UFC1 bound to EZH2 and mediated its accumulation at the promoter region of PTEN gene, resulting in the trimethylation of H3K27 and the inhibition of PTEN expression. UFC1 knockdown inhibited NSCLC growth in mouse xenograft tumor models while the simultaneous depletion of PTEN reversed this effect. NSCLC cells derived exosomes could promote NSCLC cell proliferation, migration and invasion through the transfer of UFC1. Moreover, Exosome-transmitted UFC1 promotes NSCLC progression by inhibiting PTEN expression via EZH2-mediated epigenetic silencing. Exosome-mediated transmit of UFC1 may represent a new mechanism for NSCLC progression and provide a potential marker for NSCLC diagnosis.
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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.