ArticleBioengineered2022
Role of long non-coding RNA-adducin 3 antisense RNA1 in liver fibrosis of biliary atresia.
Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- Decoding the human PBMC isonome: isoform-level resolution with single-cell long-read transcriptomics.Frontiers in genetics · 2026Article
- Decoding the human PBMC isonome: Isoform-level resolution with single-cell long-read transcriptomics.bioRxiv : the preprint server for biology · 2025Article
- LncRNAs, RNA Therapeutics, and Emerging Technologies in Liver Pathobiology.Seminars in liver disease · 2025Review
- Molecular Mechanisms of Fibrosis in Cholestatic Liver Diseases and Regenerative Medicine-Based Therapies.Cells · 2024Review
- A narrative review of genes associated with liver fibrosis in biliary atresia.Translational pediatrics · 2024Review
- Genetic Contributions to Biliary Atresia: A Developmental Cholangiopathy.Seminars in liver disease · 2023Review
- Long non-coding RNAs: key regulators of liver and kidney fibrogenesis.BMB reports · 2023Review
- mRNA and lncRNA expression profiles of liver tissues in children with biliary atresia.Experimental and therapeutic medicine · 2022Article
- Guizhi Fuling pill attenuates liver fibrosisBioengineered · 2022Article
- Loci Associated With Susceptibility to Biliary Atresia-A Genome-Wide Association Study in Taiwan.Pediatrics international : official journal of the Japan Pediatric SocietyArticle
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Biliary atresia (BA) is a devastating liver disease in neonates. Liver fibrosis is regarded as a universal and prominent feature of BA. Studies have revealed that long non-coding RNAs (lncRNAs) regulate cellular processes during the development of liver fibrosis in BA. Long non-coding RNA-adducin 3 antisense RNA1 (lnc-ADD3-AS1) has been shown to increase susceptibility to BA. However, the role of lnc-ADD3-AS1 in liver fibrosis in BA remains unclear. Here, we investigated the role of lnc-ADD3-AS1 in the proliferation, migration, and apoptosis of the immortalized human hepatic stellate cell (HSC) line, LX-2. We successfully overexpressed and silenced lnc-ADD3-AS1 in LX-2 cells using adenovirus vectors and evaluated the proliferation of transfected cells using the Cell Counting Kit-8 (CCK8) assay. Cell apoptosis was detected using annexin V-fluorescein isothiocyanate (FITC)/propidium iodide (PI) double staining and flow cytometry. We then analyzed cell migration by performing wound-scratch and transwell migration assays. Our results show that lnc-ADD3-AS1 significantly promoted LX-2 cell proliferation and attenuated apoptosis. More importantly, lncRNA-ADD3-AS1 significantly accelerated the migration of LX-2 cells. Our data indicated that lncRNA-ADD3-AS1 plays a role in the pathogenesis of liver fibrosis in patients with BA and may serve as a potential diagnostic marker for monitoring liver fibrosis in BA or as a therapeutic target for the disease.
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Registered trials
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