ArticleCell death & disease2026
AURKA-mediated destabilization of SAPS3 drives ferroptosis evasion via 7-dehydrocholesterol biosynthesis in colorectal cancer.
Article in Cell death & disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- AURKA regulates HBV-induced hepatic stellate cell inflammation and liver fibrosis by modulating K48-linked ubiquitination and proteasomal degradation of TLR3.Journal of bioenergetics and biomembranes · 2026Article
- Identification of replication factor C subunit 4 as a potential therapeutic target in esophageal squamous cell carcinoma based on bioinformatic analysis and machine learning.Discover oncology · 2026Article
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Authors and funding
9 authors.
Funding
Abstract
While ferroptosis induction offers promising avenue for cancer therapeutics, its clinical utility in colorectal cancer (CRC) is limited by pervasive intrinsic resistance mechanisms. Here, we identify Aurora kinase A (AURKA) as a central suppressor of ferroptosis by rewiring cholesterol metabolism. Mechanistically, AURKA phosphorylates and destabilizes its negative regulator SAPS3 at Ser523/524, relieving AMPK suppression. Activated AMPK subsequently inhibits SREBP2 nuclear translocation and DHCR7 transcription, resulting in the accumulation of 7-dehydrocholesterol (7-DHC), a lipid antioxidant that confers ferroptosis resistance. Both genetic and pharmacologic inhibition of AURKA restore ferroptosis sensitivity and enhance chemotherapy efficacy in vitro and in patient-derived xenograft models. Clinically, elevated AURKA expression correlates with poor prognosis and reduced chemotherapy response in CRC patients. These findings delineate a novel AURKA-SAPS3-AMPK-SREBP2 axis that bridges cholesterol homeostasis and ferroptosis evasion, positioning AURKA as a promising therapeutic target for chemosensitization in CRC.
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