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September 16, 2025Open Access

N6-methyladenosine promotes temozolomide resistance through non-canonical regulation of mRNA stability in glioblastoma cells

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Authors

EDEmily DangelmaierDFDorthy FangKHKyal Sin Htet

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Overview

Analysis reveals m6A regulates mRNA stability in glioblastoma, suggesting METTL3 inhibition may reverse resistance.

Key Points

  • N6-methyladenosine enhances temozolomide resistance in glioblastoma through mRNA stabilization.
  • Pharmacological inhibition of METTL3 destabilizes MGMT and other mRNAs, improving treatment sensitivity.
  • MGMT repair enzyme and PI3K/Akt signaling are critical pathways influenced by m6A in chemoresistance.
  • Study findings emphasize the therapeutic potential of targeting m6A methylation to combat drug resistance.

Cite This Study

Dangelmaier et al. (2025) studied this question.

synapsesocial.com/papers/68d4233c713b0b5dfea6bc71https://doi.org/10.1101/2025.09.14.676126
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1M6A RNA METHYLATION AS A THERAPEUTIC TARGET IN HIGH GRADE GLIOMA2025
  2. 2EXPLORING THE GLIOMA M6A RNA EPITRANSCRIPTOME WITH DIRECT RNA SEQUENCING2025
  3. 3Genetic and epigenetic landscape of O6-methylguanine-DNA methyltransferase (MGMT): implications for DNA repair and cancer therapeutics2025
  4. 4Novel Strategies for Improved Treatment of O6-Methylguanine-DNA Methyltransferase Promoter-Methylated Glioma2025
  5. 5NR2F6 regulates Temozolomide resistance in glioma via the E2F2-PARP1 pathway2025