Acquired resistance to EGFR-TKIs in NSCLC mediates epigenetic downregulation of MUC17 by facilitating NF-κB activity via UHRF1/DNMT1 complex
Shuye Lin, Hongyun Ruan, Lin Qin, Cong Zhao, Meng Gu, Ziyu Wang, Bin Liu, Haichao Wang, Jinghui Wang
Abstract
results also showed that DNMT1 inhibitor (5-Aza) in combination with gefitinib/osimertinib restored sensitivity to OR/GR cells. Acquired drug resistance of gefitinib/osimertinib promoted UHRF1/DNMT1 complex to inhibit the expression of MUC17. MUC17 in GR/OR cells may act as an epigenetic sensor for biomonitoring the resistance to EGFR-TKIs.
Topics & Concepts
GefitinibDNMT1OsimertinibCancer researchEpidermal growth factor receptorDNA methylationDownregulation and upregulationEpigeneticsMethyltransferaseBiologyMethylationCancerErlotinibGene expressionBiochemistryGeneticsGeneRNA modifications and cancerLung Cancer Treatments and MutationsEpigenetics and DNA Methylation