ArticleDiscover oncology2025
Mechanistic insights into Uc001kfo-induced hepatocellular carcinoma metastasis.
Article in Discover oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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
2 citing papers in PubMed.
- Decoding the functional landscape of long non-coding RNAs in hepatocellular carcinoma: molecular mechanisms, clinical implications, and therapeutic prospects.Journal of the Egyptian National Cancer Institute · 2026Review
- Noncoding RNAs: A Novel Frontier in Liver Cancer Research and Therapy: Implications for Precision Oncology.Sub-cellular biochemistry · 2026Review
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
backgroundPrevious studies have identified the long non-coding RNA (lncRNA) Uc001kfo as significantly upregulated in hepatocellular carcinoma (HCC) tissues, particularly in advanced stages, compared to adjacent non-cancerous tissues. This study aims to further explore the molecular mechanisms by which Uc001kfo promotes HCC metastasis, focusing on its regulation of α-SMA expression.
methodsThe study investigate the effects of Uc001kfo on proliferation, migration, and invasion in HCC cells using in vitro assays. Additionally, we also explored the molecular mechanism by which Uc001kfo indirectly regulates α-SMA gene transcription through its targeting of Sp1. Finally, we conducted preliminary validation in mice model to assess the potential for Uc001kfo-targeted silencing to inhibit HCC cell invasion and metastasis.
resultsThe results of the study demonstrate that the Uc001kfo/Sp1/α-SMA pathway plays a role in regulating HCC metastasis. Uc001kfo inhibits the degradation of Sp1 protein, thereby promoting Sp1 binding to the α-SMA promoter and enhancing its transcription. Consequently, silencing Uc001kfo can indirectly suppress α-SMA expression, effectively inhibiting HCC cell proliferation, invasion, and migration in vitro, as well as liver metastasis in mice through the spleen.
conclusionUc001kfo plays a critical role in promoting HCC metastasis, making it a potential a promising therapeutic target for inhibiting tumor progression and metastasis in HCC.
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Registered trials
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