Evidence map›Paper›PMID 38594783›Full record

ArticleBreast cancer research : BCR2024

U2AF2-SNORA68 promotes triple-negative breast cancer stemness through the translocation of RPL23 from nucleoplasm to nucleolus and c-Myc expression.

Wenrong Zhang, Xinyue Song, Zining Jin, Yiqi Zhang, Shan Li, Feng Jin, Ang Zheng

Open access · goldAbstract read
In one paragraph

Article in Breast cancer research : BCR, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.8field-weighted citation impact, top 9% of its field
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

14 citing papers in PubMed, 12 citations in OpenAlex.

  1. Review
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  3. mCellular & molecular biology letters · 2026
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  13. Small nucleolar RNAs: the hidden precursors of cancer ribosomes.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025
    Review
  14. 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

7 authors at 4 institutions in 1 country.

Wenrong Zhang *Department of Breast Surgery, The First Hospital of China Medical University, Shenyang, Liaoning Province, China.
Xinyue Song *Department of Pharmacology, Liaoning Province Key Laboratory of Molecular Targeted Antitumour Drug Development and Evaluation, China Medical University, Shenyang, Liaoning Province, China.
Zining Jin *Department of Breast Surgery, The First Hospital of China Medical University, Shenyang, Liaoning Province, China.
Yiqi ZhangDepartment of Breast Surgery, The First Hospital of Jinzhou Medical University, Shenyang, Liaoning Province, China.
Shan LiDepartment of General Surgery, Beijing Chao-Yang Hospital, Capital Medical University, Beijing, China.
Feng JinDepartment of Breast Surgery, The First Hospital of China Medical University, Shenyang, Liaoning Province, China. jinfeng@cmu.edu.cn.
Ang ZhengDepartment of Breast Surgery, The First Hospital of China Medical University, Shenyang, Liaoning Province, China. azheng@cmu.edu.cn.
China Medical University · CNBeijing Chao-Yang Hospital · CNFirst Hospital of China Medical University · CNJinzhou Medical University · CN

Funding

Beijing Health Promotion Association - Young Breast Surgeon Research Foundation of China CJBSRAF-2022National Natural Science Foundation of China 82073282National Natural Science Foundation of China 82203873
6 · The paper itself

Abstract

backgroundSmall nucleolar RNAs (snoRNAs) play key roles in ribosome biosynthesis. However, the mechanism by which snoRNAs regulate cancer stemness remains to be fully elucidated.

methodsSNORA68 expression was evaluated in breast cancer tissues by in situ hybridization and qRT‒PCR. Proliferation, migration, apoptosis and stemness analyses were used to determine the role of SNORA68 in carcinogenesis and stemness maintenance. Mechanistically, RNA pull-down, RNA immunoprecipitation (RIP), cell fractionation and coimmunoprecipitation assays were conducted.

resultsSNORA68 exhibited high expression in triple-negative breast cancer (TNBC) and was significantly correlated with tumor size (P = 0.048), ki-67 level (P = 0.037), and TNM stage (P = 0.015). The plasma SNORA68 concentration was significantly lower in patients who achieved clinical benefit. The SNORA68-high patients had significantly shorter disease-free survival (DFS) (P = 0.036). Functionally, SNORA68 was found to promote the cell stemness and carcinogenesis of TNBC in vitro and in vivo. Furthermore, elevated SNORA68 expression led to increased nucleolar RPL23 expression and retained RPL23 in the nucleolus by binding U2AF2. RPL23 in the nucleolus subsequently upregulated c-Myc expression. This pathway was validated using a xenograft model.

conclusionU2AF2-SNORA68 promotes TNBC stemness by retaining RPL23 in the nucleolus and increasing c-Myc expression, which provides new insight into the regulatory mechanism of stemness.

Indexed as

Triple Negative Breast NeoplasmsCarcinogenesisCell Line, TumorCell NucleusCell ProliferationGene Expression Regulation, NeoplasticHumansRNASplicing Factor U2AFRNASplicing Factor U2AFU2AF2 protein, humanRPL23SNORA68stemnessTranslocation to nucleolusTriple-negative breast cancerU2AF2

Identifiers

PMID38594783
PMCPMC11005140
OpenAlexW4394620484

What Socratic holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.