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Differential m6A methylation between parental and temozolomide resistant U87 MG cells

GSE306560 Homo sapiens Other; Expression profiling by high throughput sequencing 16 samples Submitted 2026/06/01 Platform GPL30173
Summary
N6-methyladenosine (m6A) is a critical regulator of mRNA processing and function, playing roles in mRNA processing, translation, and decay. Changes in m6A status have been implicated in various cancers, including glioblastoma (GBM), where acquired chemoresistance to temozolomide (TMZ) remains a major clinical challenge. We developed cell culture models of acquired TMZ resistance in GBM and analyzed the regulation of resistance-associated genes and pathways by m6A. We find that key resistance-associated genes and pathways are regulated by m6A methylation, including MGMT, the enzyme that repairs primary TMZ-induced DNA damage. Inhibition of METTL3 with STM2457 treatment destabilizes MGMT mRNA. Intriguingly, other TMZ resistance-associated genes are similarly regulated by m6A, suggesting that METTL3 inhibition may represent a promising therapeutic approach for overcoming TMZ resistance.
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Direct links to NCBI, no account and no request form: the whole study as GSE306560_RAW.tar, processed values as the series matrix, the supplementary file directory, and per-sample supplementary files for any of the 16 samples. Raw sequencing reads are also available from ENA.

Also filed as BioProject PRJNA1311119 and SRA study SRP612772. Searching any of these in the dataset finder brings you back here.

Study design
16 conditions, each sampled once — no replicated groups

Read from 16 sample titles: 16 distinct titles with little repetition. Check it against the sample list below before relying on it.

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