---
title: "ANO6 scaffolds ER–mitochondria contacts to sequester lipids and enable ferroptosis evasion in chem"
id: "biorxiv-4-ano6-scaffolds-er-mitochondria-contacts-to-govern-spatial-lipid"
canonical_url: "https://medichelpline.com/clinical-feed/biorxiv-4-ano6-scaffolds-er-mitochondria-contacts-to-govern-spatial-lipid"
content_type: "clinical_feed_article"
specialty: "Oncology"
source_name: "bioRxiv (Biomedical Preprints)"
source_url: "https://www.biorxiv.org/content/10.64898/2026.10.22.761200v1?rss=1"
published_at: "2026-10-23T12:00:00.000Z"
evidence_level: "Verified Feed"
license: "CC-BY-NC-4.0 / Informational Use"
---
# ANO6 scaffolds ER–mitochondria contacts to sequester lipids and enable ferroptosis evasion in chem
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/biorxiv-4-ano6-scaffolds-er-mitochondria-contacts-to-govern-spatial-lipid
- **Specialty:** [Oncology](https://medichelpline.com/clinical-feed/oncology.md)
- **Primary Source:** bioRxiv (Biomedical Preprints)
- **Source URL:** [Original Journal Publication](https://www.biorxiv.org/content/10.64898/2026.10.22.761200v1?rss=1)
- **Published At:** 2026-10-23T12:00:00.000Z
- **Evidence Rating:** Verified Feed
## Executive GIST (TL;DR)
- Investigators performed integrated multi-omic profiling of paired pre- and post-neoadjuvant chemotherapy (NAC) clinical specimens to investigate metabolic adaptations associated with resistance. - The study team engineered ANO6 models (wild-type, knockout, and conformational mutants) and applied subcellular lipidomics of purified mitochondria-associated ER membranes (**MAMs**) to map lipid compartmentalization. - Authors reported chemoresistant lesions showed increased **ANO6** expression alongside accumulation of polyunsaturated phospholipids (**PUFA-PL**) without a parallel rise in apoptosis. - Data indicated ANO6 functions beyond plasma membrane scrambling; it acts as an organelle contact scaffold at **MAMs**, coordinating ER–mitochondria tethering through a conformational activation state. - The cohort showed recruitment of vimentin (VIM) and VAPB by ANO6, assembling a VIM-ANO6-VAPB-PTPIP51 tether that couples intermediate filaments to organelle contact sites and tightens ER–mitochondria coupling. - The assembled complex routed peroxidizable lipids into cytoplasmic lipid droplets, sequestering them away from functional bilayers and thereby reducing susceptibility to **ferroptosis**. - Functional mutants differentiated scaffold activity: the I612A active conformation maintained **MAMs** integrity and lipid packaging, while the D703R scaffold-deficient mutant disrupted contact architecture. - Pharmacologic destabilization with niclosamide disrupted lipid sequestration and selectively resensitized chemoresistant cells to synthetic lethal ferroptosis in both in vitro assays and preclinical xenograft models. - The authors concluded that an ANO6-mediated structural axis at **MAMs** governs spatial lipid compartmentalization and represents a tractable metabolic vulnerability in refractory **breast cancer**. The article is a preprint and has not been peer-reviewed.
## Clinical Analysis & Structured Key Points
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Qianlu Yang 1 Yunnan Cancer Hospital; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Qianlu%2BYang%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Yang%20Q&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AQianlu%2BYang%2B) * [ORCID record for Qianlu Yang](http://orcid.org/0009-0005-5496-3712 "Open in new tab") Jie Yan 2 Affiliated Hospital of Yunnan University * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Jie%2BYan%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Yan%20J&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AJie%2BYan%2B) Ping Zhao 1 Yunnan Cancer Hospital; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Ping%2BZhao%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Zhao%20P&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3APing%2BZhao%2B) Qi Tang 1 Yunnan Cancer Hospital; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Qi%2BTang%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Tang%20Q&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AQi%2BTang%2B) Kai Zheng 1 Yunnan Cancer Hospital; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Kai%2BZheng%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Zheng%20K&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AKai%2BZheng%2B) Jiawen Zhao 1 Yunnan Cancer Hospital; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Jiawen%2BZhao%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Zhao%20J&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AJiawen%2BZhao%2B) Ziting Zhou 1 Yunnan Cancer Hospital; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Ziting%2BZhou%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Zhou%20Z&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AZiting%2BZhou%2B) Qianxi Yang 1 Yunnan Cancer Hospital; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Qianxi%2BYang%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Yang%20Q&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AQianxi%2BYang%2B) * For correspondence: yqx2018601123@outlook.com * [Abstract](https://www.biorxiv.org/content/10.64898/2026.10.22.761200v1)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_art/node:5898076/1) * [Info/History](https://www.biorxiv.org/content/10.64898/2026.10.22.761200v1.article-info)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_info/node:5898076/1) * [Metrics](https://www.biorxiv.org/content/10.64898/2026.10.22.761200v1.article-metrics)[](https://www.biorxiv.org/panels_ajax_tab/article_tab_metrics/node:5898076/1) * [Supplementary material](https://www.biorxiv.org/content/10.64898/2026.10.22.761200v1.supplementary-material)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_data/node:5898076/1) * [ Preview PDF](https://www.biorxiv.org/content/10.64898/2026.10.22.761200v1.full.pdf+html)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_pdf/node:5898076/1) ![Loading](https://www.biorxiv.org/sites/all/modules/contrib/panels_ajax_tab/images/loading.gif) ## Abstract Background: Metabolic glycerophospholipid remodeling promotes tumor persistence under neoadjuvant chemotherapy in breast cancer; however, how resistant cells evade lipotoxicity from accumulating peroxidizable lipids presents an intriguing metabolic conundrum. The underlying organelle-level spatial mechanisms remain poorly defined. Methods: Integrated multi-omic profiling of paired pre- and post-NAC clinical specimens was performed. Engineered ANO6 models (wild-type, knockout, and conformational mutants) were characterized using subcellular lipidomics of purified mitochondria-associated ER membranes (MAMs), electron microscopy, in situ proximity ligation assays, and preclinical xenograft models. Results: Chemoresistant lesions exhibited marked ANO6 upregulation and polyunsaturated phospholipid (PUFA-PL) accumulation without enhanced apoptosis. Beyond its canonical role as a plasma membrane scramblase, ANO6 operates as an organelle contact scaffold at MAMs, leveraging its conformational activation to coordinate inter-organellar tethering. ANO6 directly recruits vimentin (VIM) and VAPB to assemble a VIM-ANO6-VAPB-PTPIP51 tethering platform, structurally bridging intermediate filaments to organelle contact sites. This complex tightens ER-mitochondria coupling, establishing a specialized structural platform that routes and sequesters peroxidizable lipids into protective cytoplasmic lipid droplets, thereby shielding functional membrane bilayers from ferroptotic peroxidation. Functional dissection revealed that the active scaffolding conformation (I612A) sustains MAMs integrity and lipid packaging, whereas scaffold deficiency (D703R) compromises contact architecture. Pharmacologically perturbing this platform with niclosamide destabilized lipid sequestration, selectively resensitizing chemoresistant cells to synthetic lethal ferroptosis in vitro and in vivo. Conclusions: ANO6-mediated contact scaffolding governs spatial lipid compartmentalization, establishing the ANO6-MAMs structural axis as a potential target to exploit lipid metabolic vulnerabilities in refractory breast cancer. ### Competing Interest Statement The authors have declared no competing interest. Copyright The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a [CC-BY-NC-ND 4.0 International license](http://creativecommons.org/licenses/by-nc-nd/4.0/). bioRxiv and medRxiv thank the following for their generous financial support: > The Chan Zuckerberg Initiative, Cold Spring Harbor Laboratory, the Sergey Brin Family Foundation, California Institute of Technology, Centre National de la Recherche Scientifique, Fred Hutchinson Cancer Center, Imperial College London, Massachusetts Institute of Technology, Stanford University, The University of Edinburgh, University of Washington, and Vrije Universiteit Amsterdam. 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[ Download PDF](https://www.biorxiv.org/content/10.64898/2026.10.22.761200v1.full.pdf) Print/Save Options [Download PDF](https://www.biorxiv.org/content/biorxiv/early/2026/10/23/2026.10.22.761200.full.pdf)Full Text & In-line FiguresXML [More Info](https://www.biorxiv.org/about/FAQ#PrintOptions "More Information on Print/Save Options") [Supplementary Material ](https://www.biorxiv.org/content/10.64898/2026.10.22.761200v1.supplementary-material) [ Email](https://www.biorxiv.org/ "Email this Article") [ Share](https://www.biorxiv.org/) ANO6 Scaffolds ER Mitochondria Contacts to Govern Spatial Lipid Compartmentalization and Ferroptosis Evasion in Chemoresistant Breast Cancer Qianlu Yang, Jie Yan, Ping Zhao, Qi Tang, Kai Zheng, Jiawen Zhao, Ziting Zhou, Qianxi Yang bioRxiv 2026.10.22.761200; doi: https://doi.org/10.64898/2026.10.22.761200 This article is a preprint and has not been certified by peer review [[what does this mean?](https://www.biorxiv.org/about/FAQ#unrefereed)]. 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