ArticleFrontiers in oncology2025
XPO1-inhibitor Selinexor induces MGMT expression by activating PKA-CREB signaling in
Article in Frontiers in oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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
2 citing papers in PubMed.
- Molecular insights into DNA damage response plasticity in glioma stem cells.Communications biology · 2026Review
- Selinexor enhances temozolomide efficacy in glioblastoma through modulation of multiple resistance-associated mechanisms.Frontiers in oncology · 2026Article
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Authors and funding
8 authors.
Funding
Abstract
Purpose: The temozolomide (TMZ) resistance mechanisms in MGMT-promoter methylated Methods: A genome-wide shRNA library screen was conducted to identify genes modulating resistance in a TMZ-resistant model of MGMT-methylated U251 GBM cells. The Incucyte Device was used for live cell growth monitoring, and DNA damage was assessed by foci staining. Results: Conclusions: This study demonstrates XPO1 as a mediator TMZ resistance in MGMT-methylated GBM cells, and that MGMT expression status is a potential determinant of sensitivity to Selinexor/TMZ treatment in GBM cells. These findings also uncover a novel mechanism linking Selinexor with PKA-CREB-mediated MGMT expression, suggesting that Selinexor may enhance MGMT-dependent TMZ resistance in GBM.
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