ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
A Novel tRF, HCETSR, Derived From tRNA-Glu/TTC, Inhibits HCC Malignancy by Regulating the SPBTN1-catenin Complex Axis.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- tRNA‑derived RNAs in hepatic diseases: From biological functions to clinical translation (Review).International journal of molecular medicine · 2026Review
- Crosstalk between alternative splicing and non-coding RNAs in hepatocellular carcinoma: from regulatory mechanism to therapeutic implications.Non-coding RNA research · 2026Review
- tRNA-Derived Small RNAs in Digestive Cancers: From Translational Regulation to Immune and Extracellular Communication.Cancer science · 2026Review
- STRAP promotes hepatocellular carcinoma progression through activation of an STRAP/Wnt-β-catenin/STRAP positive feedback loop.iScience · 2026Article
- Biological functions of tsRNAs and research advances in human disease.Biochemistry and biophysics reports · 2026Review
- RNA Polymerase III-Transcribed RNAs in Health and Disease: Mechanisms, Dysfunction, and Future Directions.International journal of molecular sciences · 2025Review
- The Roles of tRNA-Derived Fragments in Cancer: Updates and Perspectives.International journal of molecular sciences · 2025Review
- A Novel tRF, HCETSR, Derived From tRNA-Glu/TTC, Inhibits HCC Malignancy by Regulating the SPBTN1-catenin Complex Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
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Authors and funding
14 authors.
Funding
Abstract
tRNA-derived fragments (tRFs), a novel class of small non-coding RNAs cleaved from transfer RNAs, have been implicated in tumor regulation. In this study, the role of a specific tRF, HCETSR is investigated, which is significantly downregulated in hepatocellular carcinoma (HCC) and correlates with advanced tumor burden and higher HCC mortality. Functional analyses revealed that HCETSR inhibits HCC malignancy and serves as an independent predictor of poor prognosis. Mechanistically, a novel SPTBN1/catenin complex axis regulated by HCETSR is identified. HCETSR binds to a critical domain of SPTBN1, disrupting its interaction with the catenin complex (comprising β-catenin, α-catenin, and P120-catenin), and facilitates the transfer of the catenin complex from the cell membrane to the nucleus. Specifically, HCETSR decreases the proteasomal degradation of β-catenin and inhibits the synthesis of nascent β-catenin. Furthermore, HCETSR suppresses the transcriptional activity of LEF1 through P120-catenin rather than α-catenin, thereby reducing β-catenin's influence on LEF1 activity. It is demonstrated that HCETSR is spliced from tRNA-Glu/TTC. The biogenesis of HCETSR and tRNA-Glu/TTC is regulated by the spliceosome and Dicer1. In conclusion, These findings suggest that HCETSR, derived from tRNA-Glu/TTC, inhibits HCC malignancy via modulation of the SPTBN1/catenin axis and may represent a promising prognostic marker and therapeutic strategy for HCC.
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