Evidence map›Paper›PMID 40123578›Full record

ArticleBiologics : targets & therapy2025

Targeting DNA Topoisomerase IIα in Retinoblastoma: Implications in EMT and Therapeutic Strategies.

Qingquan Wei, Nan Lin, Li Wang

Abstract read
In one paragraph

Article in Biologics : targets & therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

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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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

3 authors.

Qingquan WeiDepartment of Ophthalmology, Tong Ren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People's Republic of China.
Nan LinDepartment of Ophthalmology, Tong Ren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People's Republic of China.
Li WangDepartment of Ophthalmology, Tong Ren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People's Republic of China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: This study investigates the role of DNA topoisomerase IIα (TOP2A) in retinoblastoma (RB), focusing on its involvement in epithelial-mesenchymal transition (EMT) and the potential of TOP2A inhibition as a therapeutic strategy. Methods: We analyzed TOP2A expression in RB tissues using public gene expression databases (GSE97508, GSE110811, and GSE172170) and conducted functional assays in human RB cell lines (Y79 and WERI-Rb-1) modified to knock down or overexpress TOP2A. Assessments included cell proliferation, migration, invasion, and EMT marker expression via RT-PCR and Western blot. Additionally, we evaluated the effects of TOP2A modulation in subcutaneous and liver metastasis mouse xenograft models. Results: TOP2A was significantly overexpressed in RB tissues (p < 0.0001). In vitro, TOP2A knockdown inhibited RB cell proliferation, migration, and invasion, and reversed EMT marker expression (p < 0.05), while TOP2A overexpression enhanced these oncogenic processes. In vivo, TOP2A knockdown or inhibition significantly reduced tumor growth and metastasis in both subcutaneous and liver metastasis models (p < 0.05). Combination therapy with TOP2A and EMT inhibitors further enhanced anti-tumor effects, significantly reducing tumor burden and metastatic lesions (p < 0.01). Conclusion: TOP2A is pivotal in RB pathogenesis and progression, primarily by regulating EMT. Its inhibition not only curtails RB cell proliferation and metastasis but also reverses EMT, underscoring its potential as a therapeutic target. This study lays the groundwork for further exploration of TOP2A-targeted therapies in RB.

Indexed as

epithelial-mesenchymal transitionretinoblastomatargeting DNA topoisomerase IIα

Identifiers

PMID40123578
PMCPMC11929414

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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.