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Updated: Jan 16, 2026
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Oncogene Expression Analysis with Alterations in pH in a Pancreatic Ductal Cell Line
Published on: April 11, 2025
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PAFAH1B3 Exists in Linear Chromosomal and Extrachromosomal Circular DNA and Promotes HCC Progression via EMT
Dandan Li1, Huishan Sun2, Yingjie Wang3
1Department of Laboratory Medicine, State Key Laboratory of Complex Severe and Rare Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Science and Peking Union Medical College (CAMS & PUMC), Beijing 100730, China.
International Journal of Molecular Sciences
|September 27, 2025
Summary
Extrachromosomal circular DNAs (eccDNAs) like eccDNA PAFAH1B3 are increasingly found in cancer. This study shows eccDNA PAFAH1B3 promotes hepatocellular carcinoma (HCC) progression by enhancing PAFAH1B3 expression and regulating epithelial-mesenchymal transition (EMT).
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Extrachromosomal circular DNAs (eccDNAs) are implicated in various cancers.
- The specific role of eccDNAs in hepatocellular carcinoma (HCC) remains underexplored.
- PAFAH1B3 is a gene of interest in cancer biology.
Purpose of the Study:
- To investigate the abundance and function of eccDNA PAFAH1B3 in HCC.
- To determine the impact of eccDNA PAFAH1B3 on HCC cell proliferation, migration, invasion, and apoptosis.
- To elucidate the mechanism by which eccDNA PAFAH1B3 influences HCC development, including its relationship with epithelial-mesenchymal transition (EMT).
Main Methods:
- Circle-Sequencing to analyze eccDNA abundance in HCC tissues.
- Cell-based assays (EdU, Transwell, apoptosis) to assess functional effects.
- RT-PCR and Western Blot (WB) to measure gene and protein expression.
- Xenograft tumor models and immunohistochemistry (IHC) for in vivo validation.
Main Results:
- eccDNA PAFAH1B3 abundance was significantly elevated in HCC.
- Overexpression of eccDNA PAFAH1B3 promoted HCC cell proliferation, migration, and invasion, while inhibiting apoptosis.
- PAFAH1B3 mRNA levels were upregulated, and PAFAH1B3 inhibition suppressed tumor growth.
- PAFAH1B3 modulation affected EMT markers, with knockdown increasing E-cadherin and decreasing N-cadherin.
Conclusions:
- eccDNA PAFAH1B3 plays a significant role in promoting HCC occurrence and progression.
- The mechanism involves enhanced PAFAH1B3 expression and regulation of EMT.
- eccDNA PAFAH1B3 represents a potential therapeutic target for HCC.
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