ArticleCellular & molecular biology letters2025
The novel tRNA-derived fragment, tiRNA-Met, inhibits the malignant progression of triple-negative breast cancer by regulating RANBP3L via a targeted interaction with SNRPA.
Article in Cellular & molecular biology letters, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- tRF-18-8R1546D2 is upregulated in hepatocellular carcinoma and associated with poor prognosis and tumor progression.Clinical and experimental medicine · 2026Article
- Harnessing Ribonucleoprotein Granule Biology for Cancer Therapy: The Central Role of Protein Modifications.Research (Washington, D.C.) · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
backgroundtRNA-derived fragments (tRFs) have emerged as significant noncoding RNAs in cancer biology; however, their roles and mechanisms in triple-negative breast cancer (TNBC) remain inadequately characterized.
methodstRF and tiRNA sequencing, real-time quantitative polymerase chain reaction (RT-qPCR), fluorescence in situ hybridization (FISH), and subcellular fractionation were used to explore the expression and characteristic of tiRNA-Met in TNBC. The biological functions of tiRNA-Met were assessed using CCK-8 assays, colony formation assays, and Transwell assays in vitro, alongside mouse xenograft models in vivo. RNA pull-down, mass spectrum, RNA immunoprecipitation (RIP), western blot, ubiquitination assays, RNA sequencing, actinomycin D assays, immunofluorescence, immunohistochemical staining, and rescue experiments were performed to explore the regulatory mechanisms of tiRNA-Met in TNBC.
resultstiRNA-Met was an uncharacterized tRF that originated from mitochondrial tRNA
conclusionsOur study identified tiRNA-Met as a novel anti-oncogenic tRF and elucidated its mechanism for inhibiting the malignancy of TNBC. tiRNA-Met directly bound to SNRPA, promoting its degradation and stabilizing RANBP3L mRNA, ultimately leading to the inhibition of the mTORC1 signaling pathway. These findings position tiRNA-Met as a promising candidate for diagnostic and therapeutic applications in TNBC.
Indexed as
Identifiers
What Socratic 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 Socratic graph.