ArticleiScience2026
NUP62 promotes breast cancer progression and inhibits ferroptosis by stabilizing NRF2 in a KEAP1-dependent way.
Article in iScience, 2026. 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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10 authors.
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Abstract
Identification of drug resistance drivers of breast cancer (BC) is a multifaceted challenge. Here, we demonstrated that NUP62 is significantly upregulated in BC tissues and cell lines, and its high expression correlates with a poor prognosis. Functional experiments revealed that NUP62 promotes BC cell proliferation, migration, and malignant phenotypes, while inhibiting ferroptosis. Mechanistically, NUP62 competitively binds to KEAP1, disrupting KEAP1-mediated ubiquitination and degradation of NRF2. This stabilization promotes NRF2 nuclear translocation, enhancing the transcription of antioxidant genes and inhibiting ferroptosis. Crucially, eribulin-identified through virtual screening of FDA-approved compounds-selectively inhibited NUP62, destabilizing NRF2 and abrogating its nuclear localization.
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