ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026
Low YTHDC1 Expression Upregulates FSCN1 to Promote Nuclear F-Actin Formation and Facilitate Double-strand DNA Breaks Repair in TMZ-Resistant Glioblastoma.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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
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.
Who cites it
2 citing papers in PubMed.
- 4H-CRCXL Mitigates RasV12-Induced Phenotypes in Glioblastoma Model of Drosophila.Molecular carcinogenesis · 2026Article
- Multidrug resistance in cancer: current understandings and future perspective.Molecular biomedicine · 2026Review
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Glioblastoma (GBM) is an aggressive and recurrent malignancy with a poor prognosis. Although temozolomide (TMZ) is a cornerstone of GBM treatment, its efficacy is often compromised by inherent or acquired resistance, underscoring the urgent need to uncover molecular mechanisms, discover new therapeutic targets, and develop innovative treatment strategies. In this study, we found an increased formation of filamentous actin (F-actin) within the nuclei of TMZ-resistant GBM cells. We also showed that overexpression of FSCN1 in TMZ-resistant GBM cells promotes F-actin formation and facilitates the repair of DNA double-strand breaks (DSBs). Further investigation revealed a marked decrease in the expression of YTHDC1 in TMZ-resistant GBM cells, which regulates FSCN1 through m6A modification. Additionally, FSCN1 activates the CDC42/N-WASP/Arp2/3 signaling pathway by recruiting FGD1 to activate CDC42
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