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December 23, 2025Molecular BiomedicineOpen Access

FOSL1-PRMT1 transcriptional-epigenetic circuit promotes glioblastoma radioresistance via calcyphosine-mediated DNA repair and invasion

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Authors

YZYating ZhangJTJiajia TianSWShuai Wu

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Overview

Targeting FOSL1-PRMT1 may improve radiosensitivity and reduce tumor invasion in glioblastoma patients, suggesting a new therapeutic strategy.

Key Points

  • The research aims to understand the molecular mechanisms of radioresistance in glioblastoma and the role of the FOSL1-PRMT1-CAPS axis.
  • Identified FOSL1 as a key driver of glioblastoma radioresistance.
  • Examined the interactions between FOSL1, PRMT1, and Calcyphosine (CAPS).
  • Utilized an orthotopic GBM mouse model to test genetic and pharmacological disruptions of the signaling axis.
  • FOSL1 knockdown sensitized glioblastoma cells to irradiation and reduced DNA damage repair.
  • The FOSL1-PRMT1-CAPS axis enhanced both Homologous Recombination and Non-Homologous End Joining pathways.
  • Disruption of this axis increased radiosensitivity and decreased tumor invasion in mouse models.

Cite This Study

Zhang et al. (2025) studied this question.

synapsesocial.com/papers/6949ddb572f746a93d78903ahttps://doi.org/10.1186/s43556-025-00394-0
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