ArticleScientific reports2025
TET2 repression contributes to EGFR TKI resistance in EGFR-mutant non-small cell lung cancer through regulating AXIN2 methylation.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Through targeted next-generation sequencing of 83 non-small cell lung cancer (NSCLC) patients with first-generation epidermal growth factor receptor tyrosine kinase inhibitor (EGFR TKI) resistance, we detected 11% TET2 mutations in the T790M-negative subgroup. To explore the molecular mechanism of TET2 in EGFR TKI resistance, reduced representation bisulfite sequencing (RRBS) was adopted to analyze the global genomic methylation profiles and detect the differentially methylated genes in the TET2-knockdown (KD) PC9 and control PC9 cell lines, following bioinformatics analysis of gene ontology (GO) functions and kyoto encyclopedia of genes and genomes (KEGG) signaling to screen for genes associated with drug resistance. TET2 KD attenuated gefitinib-induced apoptosis and decreased the sensitivity of EGFR-mutant lung cancer cells to gefitinib. Forty-three drug resistance genes with hypermethylated promoter regions were identified via RRBS and bioinformatic analysis in PC9
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