ArticleInternational journal of molecular sciences2025
PAFAH1B3 Exists in Linear Chromosomal and Extrachromosomal Circular DNA and Promotes HCC Progression via EMT.
Article in International journal of molecular sciences, 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
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Who cites it
2 citing papers in PubMed.
- Extrachromosomal DNA as a platform for epigenetic reprogramming in cancer.Molecular cancer · 2026Review
- Identification of key genes as diagnostic biomarkers for lung adenocarcinoma using bioinformatics and machine learning.Discover oncology · 2026Article
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Authors and funding
10 authors.
Funding
Abstract
Recent evidence highlights the role of extrachromosomal circular DNAs (eccDNAs) in cancers. However, reports regarding its role in hepatocellular carcinoma (HCC) are infrequent. The abundance of eccDNAs from five HCC/adjacent tissue pairs was explored using Circle-Sequencing. eccDNA PAFAH1B3 was selected as one of the objects. The effect of eccDNA PAFAH1B3 on HCC progression was determined using EdU, Transwell, and apoptosis assays. Additionally, the expressions of eccDNA PAFAH1B3, mRNA PAFAH1B3, and epithelial-mesenchymal transition (EMT)-related markers were determined using RT-PCR and WB. A xenograft tumor model was established to explore the function of PAFAH1B3 in vivo, and EMT-related markers were detected using RT-PCR and IHC analyses. The abundance of eccDNA PAFAH1B3 was significantly increased in HCC cell lines after transfection with eccDNA PAFAH1B3, and promoted the proliferation, migration, and invasion of liver cells while inhibiting apoptosis. The levels of mRNA PAFAH1B3 were also upregulated. Furthermore, intratumoral injection of PAFAH1B3 inhibitor suppressed tumor growth, and PAFAH1B3 knockdown increased and decreased the levels of the E-cadherin and N-cadherin, respectively. Our study findings reveal that eccDNA PAFAH1B3 may promote the occurrence and development of HCC by enhancing the expression of PAFAH1B3 and regulating EMT.
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