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- W4313887277 abstract "Drug resistance has become a challenge in effective longterm molecular targeted therapy. Longterm non-small cell lung cancer (NSCLC) treatments with the first-generation epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) shorten the effective duration of the third-generation EGFR-TKI, osimertinib, via genetic or epigenetic mechanisms in addition to the gatekeeper mutation T790M. This study reproduced this persistence in vitro using gefitinib-resistant NSCLC PC-9 cells (GR cells) and revealed that pharmacological nuclear localization inhibition of β-catenin suppressed the osimertinib resistance. Osimertinib effectively reduced GR cell survival but left significantly more resistant colonies than parental PC-9 cells. The nuclear fraction of β-catenin was enriched in GR cells during acquisition of osimertinib resistance. A chemical nuclear localization inhibitor of β-catenin, IMU1003, dramatically decreased the emergence of osimertinib-resistant colonies. Forced nuclear localization of β-catenin reduced IMU1003 efficacy. Thus, suppression of the nuclear β-catenin function may overcome the transgenerational EGFR-TKI-resistance." @default.
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- W4313887277 date "2023-02-01" @default.
- W4313887277 modified "2023-10-15" @default.
- W4313887277 title "A Wnt/β-catenin signaling inhibitor, IMU1003, suppresses the emergence of osimertinib-resistant colonies from gefitinib-resistant non-small cell lung cancer cells" @default.
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- W4313887277 doi "https://doi.org/10.1016/j.bbrc.2023.01.018" @default.
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