ArticleExperimental & molecular medicine2024
Role of UPF1 in lncRNA-HEIH regulation for hepatocellular carcinoma therapy.
Article in Experimental & molecular medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- LINC00839 transcriptionally activated by ELK1 represses ferroptosis in nasopharyngeal carcinoma by regulating UPF1/RCHY1/DJ-1 axis.NPJ precision oncology · 2026Article
- Long non-coding RNA in hepatocellular carcinoma: mechanistic insights and therapeutic perspectives.Cellular oncology (Dordrecht, Netherlands) · 2025Review
- Identification of palmitoylation-related lncRNAs as prognostic biomarkers and immune modulators in HCC.Discover oncology · 2025Article
- Evolving roles for the androgen receptor and its protein interactome in castration-resistant prostate cancer.Oncogene · 2025Review
- The role of exosomes in liver cancer: comprehensive insights from biological function to therapeutic applications.Frontiers in immunology · 2024Review
- [Long noncoding RNA HClnc1 promotes proliferation and migration of liver cancer cells by targeting RBBP5/KAT2B complex to enhance ODC1 transcription].Nan fang yi ke da xue xue bao = Journal of Southern Medical UniversityArticle
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
UPF1, a novel posttranscriptional regulator, regulates the abundance of transcripts, including long noncoding RNAs (lncRNAs), and thus plays an important role in cell homeostasis. In this study, we revealed that UPF1 regulates the abundance of hepatocellular carcinoma upregulated EZH2-associated lncRNA (lncRNA-HEIH) by binding the CG-rich motif, thereby regulating hepatocellular carcinoma (HCC) tumorigenesis. UPF1-bound lncRNA-HEIH was susceptible to degradation mediated by UPF1 phosphorylation via SMG1 and SMG5. According to analysis of RNA-seq and public data on patients with liver cancer, the expression of lncRNA-HEIH increased the levels of miR-194-5p targets and was inversely correlated with miR-194-5p expression in HCC patients. Furthermore, UPF1 depletion upregulated lncRNA-HEIH, which acts as a decoy of miR-194-5p that targets GNA13, thereby promoting GNA13 expression and HCC proliferation. The UPF1/lncRNA-HEIH/miR-194-5p/GNA13 regulatory axis is suggested to play a crucial role in cell progression and may be a suitable target for HCC therapy.
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