ArticleInternational journal of clinical and experimental pathology2020
miR-103 promotes hepatocellular carcinoma cell proliferation and migration in the simulation transition zone of RFA through PI3K/Akt signaling pathway by targeting PTEN.
Article in International journal of clinical and experimental pathology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 7 citations in OpenAlex.
- Post-ablation recurrence in hepatocellular carcinoma: molecular pathogenesis and targeted therapeutic innovations.American journal of cancer research · 2025Review
- Emerging role of MicroRNA-Based theranostics in Hepatocellular Carcinoma.Molecular biology reports · 2023Review
- MiR-103a promotes tumour growth and influences glucose metabolism in hepatocellular carcinoma.Cell death & disease · 2021Article
- Review
- Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Radiofrequency ablation (RFA) is a potentially curative therapy for nontransplantable hepatocellular carcinoma (HCC). However, as tumor size increases, incomplete RFA can increase rates of local recurrence and tumor progression. As such, there remains a need to identify potential biologic mechanisms mediating HCC response to thermal ablation. Our results revealed that miR-103 was markedly upregulated in recurrent HCC tissues treated with RFA as first-line treatment and in HCC lines after heat stress in vitro, simulating the marginal zone of RFA treatment. Gain-of-function and loss-of-function studies showed that miR-103 ectopic overexpression promoted, but miR-103 silencing reduced, heat-exposed HCC proliferation, and migration in vitro. Western blotting displayed that proteins related with proliferation and migration were significantly changed in different groups. Furthermore, PTEN may be a potential target of miR-103 and miR-103 could activate the PI3K/Akt pathway by suppressing PTEN expression. Taken together, these studies provide experimental evidence supporting a role for miR-103 in HCC response to heat stress.
Indexed as
Identifiers
32269684PMC7137015W3017926059What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.