Anoctamin 6 scaffolds ER-mitochondria contacts to help chemoresistant breast cancer evade ferroptosis
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A preprint posted to bioRxiv on October 23, 2026 reports that ANO6 is upregulated in chemotherapy-resistant breast cancer lesions. The protein acts through a VIM-ANO6-VAPB-PTPIP51 scaffold at endoplasmic reticulum-mitochondria contact sites, where it sequesters peroxidizable lipids. By compartmentalizing these lipids away from sites where they could be oxidized, the scaffold allows resistant cancer cells to evade ferroptosis, a form of lipid-peroxidation-driven cell death. The work positions ANO6-mediated organelle contact remodeling as a mechanism of chemotherapy resistance in breast cancer. The findings are currently a Cancer Biology preprint and have not yet undergone peer review or journal publication.
Written by a model from the reports · updated 3 hours ago
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- biorxiv.orgANO6 Scaffolds ER Mitochondria Contacts to Govern Spatial Lipid Compartmentalization and Ferroptosis Evasion in Chemoresistant Breast Cancer
The study shows that ANO6 is upregulated in chemotherapy-resistant breast cancer lesions. Through the VIM-ANO6-VAPB-PTPIP51 scaffold at ER-mitochondria contact sites, ANO6 sequesters peroxidizable lipids and thereby evades ferroptosis.
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