This work highlights how detailed, transcript-level dissection of RNA modification-driven regulation can expose unexpected, yet clinically actionable mechanisms. Big shoutouts to Emily in the lab for spearheading the effort, and to the NIH and Sontag Foundations for $$$ support!

Blocking m6A installation by inhibiting METTL3 restored chemosensitivity by diminishing expression of transcripts associated with temozolomide resistance, including MGMT, a DNA repair enzyme and critical prognostic marker of poor therapy response in glioblastoma.

We found that m6A promotes therapy resistance by stabilizing a specific subset of transcripts which are upregulated in glioma cells with acquired resistance to temozolomide.

Using a combination of:
✅ Chemoresistant glioblastoma cell culture models
✅ RNA-seq
✅ m6A-eCLIP
we explored how m6A shapes transcriptomic reprogramming as glioblastoma cells adapt to chemotherapy.