ArticleCell death & disease2025
LncRNA EP300-AS1 interacts with PTBP1 to destabilize PRMT5 mRNA and suppresses NSCLC growth and metastasis.
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 2 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- A novel antisense lncRNA, LPCRL, functions as a molecular scaffold for the USP15/MIB1 complex to promote primary cisplatin resistance and tumor progression in lung squamous cell carcinoma.Journal of experimental & clinical cancer research : CR · 2026Article
- Research progress on long non‑coding RNAs in lung cancer (Review).Molecular medicine reports · 2026Review
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Authors and funding
4 authors.
Funding
Abstract
Non-small-cell lung cancer (NSCLC) is one of the most common types of malignant cancer, characterized by high rates of metastasis and mortality. However, the molecular mechanisms underlying NSCLC growth and progression remain largely unclear. Here, EP300-AS1 is identified as a critical tumor-suppressive long non-coding RNA (lncRNA) in NSCLC. EP300-AS1 inhibits NSCLC cell growth and metastasis both in vitro and in vivo, and is associated with better clinical outcomes. The function of EP300-AS1 depends on EP300-AS1-PTBP1 interaction and PTBP1-mediated PRMT5 mRNA stability. EP300-AS1 binds directly to PTBP1, preventing its cytoplasmic translocation and PTBP1-PRMT5 mRNA complex formation in NSCLC. In the absence of PTBP1 binding to the PRMT5 mRNA 3'-UTR, PRMT5 mRNA stability and expression are reduced. PTBP1 knockdown or PRMT5 inhibition abolishes EP300-AS1-regulated NSCLC cell proliferation, migration, and invasion. In patients with lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC), EP300-AS1 expression is negatively correlated with PRMT5 expression. Overall, these findings establish the EP300-AS1-PTBP1-PRMT5 axis as a key regulatory pathway in NSCLC progression, providing a novel regulatory mechanism and a promising target for NSCLC prediction and therapy.
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Registered trials
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