Evidence map›Paper›PMID 39711373›Full record

ReviewAnnals of medicine2025

RNA-binding protein quaking: a multifunctional regulator in tumour progression.

Wangyu Zhu, Weiwei Yang, Guoping Sun, Jian Huang

Abstract readReview
In one paragraph

Review in Annals of medicine, 2025. 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
–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

14 citing papers in PubMed.

  1. Article
  2. Animals : an open access journal from MDPI · 2026
    Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Review
  8. Review
  9. Review
  10. RNA-Binding Proteins: Modulators of Canonical Wnt Signaling Pathway.International journal of molecular sciences · 2025
    Review
  11. Review
  12. Article
  13. 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

4 authors.

Wangyu ZhuCell and Molecular Biology Laboratory, Zhoushan Hospital of Wenzhou Medical University, Zhoushan, Zhejiang, China.ORCID 0000-0003-4805-0800
Weiwei YangCell and Molecular Biology Laboratory, Zhoushan Hospital of Wenzhou Medical University, Zhoushan, Zhejiang, China.
Guoping SunDepartment of Breast Surgery, Second Affiliated Hospital and Cancer Institute (Provincial Key Laboratory of Tumor Microenvironment and Immunotherapy, Key Laboratory of Cancer Prevention & Intervention, National Ministry of Education), Zhejiang University School of Medicine, Hangzhou, China.
Jian HuangDepartment of Breast Surgery, Second Affiliated Hospital and Cancer Institute (Provincial Key Laboratory of Tumor Microenvironment and Immunotherapy, Key Laboratory of Cancer Prevention & Intervention, National Ministry of Education), Zhejiang University School of Medicine, Hangzhou, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundQuaking (QKI) is a member of the signal transduction and activators of RNA (STAR) family, performing a crucial multifunctional regulatory role in alternative splicing, mRNA precursor processing, mRNA transport and localization, mRNA stabilization, and translation during tumour progression. Abnormal QKI expression or fusion mutations lead to aberrant RNA and protein expression, thereby promoting tumour progression. However, in many types of tumour, QKI played a role as tumour suppressor, the regulatory role of QKI in tumour progression remains ambiguous.

objectivesThis review aims to analyze the isoform and function of QKI, the impact of QKI-regulated gene expression or signalling pathway alterations on tumour progression, and its potential clinical applications as a predictive marker or target for tumour therapy.

methodsWe reviewed recent studies and summarized the function of QKI alteration in tumour progression.

resultsQKI mediate post-transcriptional gene regulation including alternative splicing, polyadenylation, mRNA stabilization, mRNA subcellular location, and noncoding RNA by binding to the QRE elements of targeted nucleotide. The dysregulation of QKI is intricately correlated to tumour proliferation, metastasis, angiogenesis, tumor stem cells, the tumour microenvironment, and treatment sensitivity, and represents as a potential biological predictor in tumour diagnosis and prognosis.

conclusionsQKI play a critical role as tumour suppressor or an oncogene in tumour progression due to the different splicing sites and transcripts with various tumour subtype or tumor micorenvironment. Ongoing research about QKI's functions and mechanisms persist is required to conduct for better understanding the role of QKI in tumour regulation.

Indexed as

Disease ProgressionGene Expression Regulation, NeoplasticNeoplasmsRNA-Binding ProteinsAlternative SplicingHumansRNA, MessengerSignal TransductionTumor MicroenvironmentQKI protein, humanRNA-Binding ProteinsRNA, Messengerpost-translational regulationQKItumour progression

Identifiers

PMID39711373
PMCPMC11703483

What Socratic holds

Textmetadata
LicenceCC BY-NC
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.