ArticleJournal of molecular neuroscience : MN2023
SRSF4 Confers Temozolomide Resistance of Glioma via Accelerating Double Strand Break Repair.
Article in Journal of molecular neuroscience : MN, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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Who cites it
1 citing paper in PubMed, 5 citations in OpenAlex.
- Multidimensional regulatory roles and therapeutic applications of SRSF7 in cancer.Cell death discovery · 2025Review
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7 authors at 3 institutions in 1 country.
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Abstract
Temozolomide (TMZ)-based chemotherapy plays a central part in glioma treatment. However, prominent resistance to TMZ is a major change by now. In this study, expression and prognosis of SRSF4 were analyzed using multiple public datasets. Therapeutic efficacy against TMZ resistance was determined by assessing colony formation, flow cytometry, and western blot assays. Bio-informational analysis, immunofluorescence (IF), and western blot assays were performed to evaluate double strand break repair. An orthotopic xenograft model was used to exam the functional role of SRSF4. Here, we found that SRSF4 expression was associated with histological grade, IDH1 status, 1p/19q codeletion, molecular subtype, tumor recurrence, and poor prognosis. SRSF4 promotes TMZ resistance through positively regulating MDC1, thereby accelerating double strand break repair. Targeting SRSF4 could significantly improve chemosensitivity. Taken together, our collective findings highlight an important role of SRSF4 in the regulation of TMZ resistance by modulation of double strand break repair.
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