ArticleDiscover oncology2026
ELK3 promotes cisplatin resistance in ovarian cancer via regulating CHD4 gene expression.
Article in Discover oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
The trial behind it
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Who cites it
1 citing paper in PubMed.
- ETS transcription factor ELK3: Molecular insights and translational horizons in cancer (Review).Oncology letters · 2026Review
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Authors and funding
6 authors.
Funding
Abstract
backgroundCisplatin resistance remains a major obstacle in the treatment of ovarian cancer (OC). Although ELK3, an ETS transcription factor, has been implicated in chemoresistance across various cancers, its specific role and molecular mechanisms in OC progression and cisplatin resistance remain poorly understood.
methodsELK3 expression was analyzed in cisplatin-resistant OC cells using qPCR and Western blotting. Functional assays, including CCK-8, apoptosis analysis, and xenograft models, were employed to assess the impact of ELK3. Mechanistic insights were gained through Co-IP and histone lactylation analysis.
resultsELK3 was significantly upregulated in cisplatin-resistant OC tissues and cells, and its elevated expression correlated with poor patient survival according to TCGA and KM Plotter data. Knockdown of ELK3 sensitized OC cells to cisplatin by suppressing CHD4 expression and reducing histone lactylation levels. Importantly, restoration of CHD4 expression rescued cisplatin resistance in ELK3-deficient cells.
conclusionThe ELK3-CHD4-histone lactylation axis plays a critical role in driving cisplatin resistance in OC, highlighting its potential as a novel therapeutic target for overcoming chemoresistance.
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