Evidence map›Paper›PMID 40096176›Full record

ArticlePLoS genetics2025

TRIM21 modulates stability of pro-survival non-coding RNA vtRNA1-1 in human hepatocellular carcinoma cells.

EunBin Kong, Norbert Polacek

Abstract read
In one paragraph

Article in PLoS genetics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

4 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

EunBin KongDepartment for Chemistry, Biochemistry and Pharmaceutical Sciences, University of Bern, Bern, Switzerland.
Norbert PolacekDepartment for Chemistry, Biochemistry and Pharmaceutical Sciences, University of Bern, Bern, Switzerland.ORCID https://orcid.org/0000-0001-5317-3990

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent studies expanded our knowledge of diverse pro-survival functions of short non-coding vault RNAs. One of the human vault RNA paralogs, vtRNA1-1, modulates several intracellular processes, including proliferation, apoptosis, autophagy, and drug resistance in various types of human cancer cells. However, protein interaction partners and mechanisms by which vtRNA1-1 levels are controlled within the cells remained elusive. Here, we describe a regulatory process for vtRNA1-1 stabilization mediated by the newly identified interacting proteins, TRIM21 and TRIM25, in human hepatocellular carcinoma (HCC) cells. Depleting TRIM21 or TRIM25 reduced the stability of vtRNA1-1 both in vivo and in vitro. We also identified the responsible sequence of vtRNA1-1 for the stability regulation by TRIM21 and TRIM25 and revealed another critical factor for vtRNA1-1 stability, an NSUN2-mediated methylation at C69 of vtRNA1-1. Consequently, our findings demonstrated that the TRIM proteins govern the stability of vtRNA1-1 depending on its methylation status in HCC cells. Since vtRNA1-1 is crucial for pro-survival characteristics in HCC cells, insight into vtRNA1-1 protein binding partners and the regulation of its stability can impact the development of new anticancer strategies.

Indexed as

Carcinoma, HepatocellularLiver NeoplasmsRNA, UntranslatedApoptosisCell Line, TumorCell ProliferationCell SurvivalGene Expression Regulation, NeoplasticHumansMethylationMethyltransferasesRibonucleoproteinsRNA StabilitySS-A AntigenTranscription FactorsTripartite Motif ProteinsMethyltransferasesNSUN2 protein, humanRibonucleoproteinsRNA, UntranslatedSS-A AntigenTranscription FactorsTRIM25 protein, humanTripartite Motif ProteinsUbiquitin-Protein Ligases

Identifiers

PMID40096176
PMCPMC11940608

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Registered trials

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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.