ArticleJournal of translational medicine2025
LncRNA PVT1 activated by TGF-β1/Smad3 facilitates proliferation and metastasis of hepatocellular carcinoma via upregulating Smad6 and NRG1.
Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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Who cites it
1 citing paper in PubMed.
- Long Non-Coding RNAs in Human Disease: An Overview of Biogenesis, Molecular Mechanism and Therapeutic Opportunities.Current issues in molecular biology · 2026Review
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10 authors.
Funding
Abstract
backgroundHepatocellular carcinoma (HCC) significantly affects the patient's physical and mental health. Long non-coding RNA plasmacytoma variant translocation 1 (lncRNA PVT1) has been associated with the progression of HCC. However, the current effectiveness of HCC treatment is considered insufficient, and the scope of its therapeutic targets is highly limited. The purpose of this investigation is to investigate the pathogenic mechanism of PVT1 in HCC and assess its potential for gene therapy in HCC.
methodsThis study assessed cycle phases and proliferative capacity of HCC cells through flow cytometry, CCK-8 assay, EdU, and colony formation assays. Chromatin Immunoprecipitation (ChIP) and Dual-Luciferase Reporter Assays were conducted to investigate the interactions among the promoter and PVT1, PVT1 and its target miRNAs, as well as miRNAs and their target genes. BALB/c nude mice were employed to establish models for studying the proliferation and metastasis of HCC in vivo.
resultsThe data revealed that TGF-β1 upregulates PVT1, while Smad3 functions as a transcription factor to modulate PVT1. PVT1, in turn, upregulates Smad6 and NRG1 (Neuregulin 1). Moreover, PVT1 combines with miR-186-5p and miR-143-3p, while miR-186-5p inhibits Smad6 and miR-143-3p inhibits NRG1. Further, in vivo and in vitro analyses revealed that PVT1 stimulates the expression of Smad6, thereby promoting the proliferation of HCC. In addition, PVT1 also promotes the spread of HCC by upregulating NRG1.
conclusionThis study validated that PVT1 activated by TGF-β1/Smad3 facilitates HCC progression and metastasis by upregulating the miR-186-5p/Smad6 and miR-143-3p/NRG1 axes, indicating its potential as a biological target for treating HCC.
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