Evidence map›Paper›PMID 40555777›Full record

ArticleBritish journal of cancer2025

Spliceosomal GTPase EFTUD2 mediates DDX41 intron retention to promote the malignant progression of ovarian cancer.

Yanling Liu, Zhongshao Chen, Yan Duan, Zixian Shao, Yuliang Chen, Ning Yang, Huimin Xiao, Yingwei Li, Kun Song

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in British journal of cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
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

9 authors.

Yanling LiuDepartment of Obstetrics and Gynecology, Qilu Hospital of Shandong University, Shandong Key Laboratory of Reproductive Health and Birth Defects Prevention and Control, Ji'nan, Shandong Province, China.
Zhongshao ChenDepartment of Obstetrics and Gynecology, Qilu Hospital of Shandong University, Shandong Key Laboratory of Reproductive Health and Birth Defects Prevention and Control, Ji'nan, Shandong Province, China.
Yan DuanDepartment of Obstetrics and Gynecology, Shengli Oilfield Central Hospital, Dongying, Shandong Province, China.
Zixian ShaoDepartment of Obstetrics and Gynecology, Qilu Hospital of Shandong University, Shandong Key Laboratory of Reproductive Health and Birth Defects Prevention and Control, Ji'nan, Shandong Province, China.
Yuliang ChenDepartment of Obstetrics and Gynecology, Qilu Hospital of Shandong University, Shandong Key Laboratory of Reproductive Health and Birth Defects Prevention and Control, Ji'nan, Shandong Province, China.
Ning YangDepartment of Obstetrics and Gynecology, Qilu Hospital of Shandong University, Shandong Key Laboratory of Reproductive Health and Birth Defects Prevention and Control, Ji'nan, Shandong Province, China.
Huimin XiaoDepartment of Obstetrics and Gynecology, Qilu Hospital of Shandong University, Shandong Key Laboratory of Reproductive Health and Birth Defects Prevention and Control, Ji'nan, Shandong Province, China.
Yingwei LiDepartment of Obstetrics and Gynecology, Qilu Hospital of Shandong University, Shandong Key Laboratory of Reproductive Health and Birth Defects Prevention and Control, Ji'nan, Shandong Province, China. sduliyingwei@126.com.ORCID http://orcid.org/0000-0002-1155-221X
Kun SongDepartment of Obstetrics and Gynecology, Qilu Hospital of Shandong University, Shandong Key Laboratory of Reproductive Health and Birth Defects Prevention and Control, Ji'nan, Shandong Province, China. songkun2001226@sdu.edu.cn.ORCID http://orcid.org/0000-0001-6110-2770

Funding

Natural Science Foundation of Shandong Province (Shandong Provincial Natural Science Foundation) ZR2023MH183
6 · The paper itself

Abstract

backgroundDysregulation of alternative splicing (AS) has been identified as a promising target for cancer therapy. Nevertheless, the precise molecular mechanisms by which AS influences ovarian cancer (OC) progression have not yet been fully elucidated.

methodsA comprehensive bioinformatics analysis was conducted to identify and screen core splicing factors in OC. The splicing factor EFTUD2 was found to be significantly overexpressed in clinical OC samples. Subsequent in vitro and in vivo assays elucidated the oncogenic role of EFTUD2 in OC. RNA-seq and AS events analysis were employed to determine the key downstream target regulated by EFTUD2. ASOs targeting EFTUD2 were developed for efficacy validation.

resultsEFTUD2 was identified as a critical splicing factor in the pathogenesis of OC, and EFTUD2 knockdown impeded OC tumorigenesis and progression. The EFTUD2-ASO significantly inhibited tumor growth in vivo. Mechanistically, EFTUD2 was shown to promote the malignant biological behavior of OC by facilitating the efficient splicing of DDX41 and maintaining the oncogenic expression of its functional proteins. Knockdown of DDX41 partially mitigated the EFTUD2-induced malignant progression of OC cells.

conclusionsOur findings suggest that the EFTUD2/DDX41 axis is a viable target for OC. ASO-mediated silencing of EFTUD2 presents promising new therapeutic options for OC patients.

Indexed as

DEAD-box RNA HelicasesOvarian NeoplasmsPeptide Elongation FactorsRibonucleoprotein, U5 Small NuclearSpliceosomesAlternative SplicingAnimalsCell Line, TumorCell ProliferationDisease ProgressionFemaleGene Expression Regulation, NeoplasticHumansIntronsMiceMice, NudeDEAD-box RNA HelicasesEFTUD2 protein, humanPeptide Elongation FactorsRibonucleoprotein, U5 Small Nuclear

Identifiers

PMID40555777
PMCPMC12356982

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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.