Xanthine oxidoreductase (XOR) is identified as a key mediator of resistance to EGFR tyrosine kinase inhibitors (TKIs) in intrahepatic cholangiocarcinoma (iCCA).
XOR promotes EGFR protein stability via USP8-mediated deubiquitination and upregulates MUC1, enhancing oncogenic signaling and DNA damage repair.
Knockdown or inhibition of XOR reduces tumor proliferation, exacerbates DNA damage, and significantly increases sensitivity of iCCA cells to EGFR TKIs like gefitinib.
Targeting XOR offers a novel therapeutic strategy to overcome TKI resistance and improve outcomes in patients with iCCA, an aggressive liver cancer with limited treatment options.
Study Background
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This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.
