Abstract
Cancer cells regulate cholesterol levels to sustain proliferation and metabolic adaptation. Here, we show that TMEM97 coordinates cholesterol sensing with oxidative phosphorylation in gastric cancer. Loss of TMEM97 reduced in vitro proliferation and impaired xenograft tumor growth. TMEM97 deficiency disrupted cholesterol homeostasis, causing accumulation of the post-lanosterol intermediate follicular fluid meiosis-activating sterol (FF-MAS) under both normal and lipoprotein-deficient serum conditions. Metabolomic and transcriptomic analyses further revealed altered tricarboxylic acid (TCA) cycle activity under lipoprotein-deficient conditions. Structural analysis identified a conserved cholesterol recognition amino acid consensus (CARC) motif in TMEM97, and its deletion reduced cholesterol binding. Collectively, TMEM97 regulates sterol regulatory element binding protein (SREBP)-associated lipid programs, post-lanosterol cholesterol biosynthesis, and mitochondrial bioenergetics. These findings identify TMEM97 as a regulator of cholesterol-dependent metabolic adaptation in gastric cancer and support TMEM97-associated cholesterol regulation as a potential therapeutic vulnerability.
| Original language | English |
|---|---|
| Article number | 116773 |
| Journal | iScience |
| Volume | 29 |
| Issue number | 8 |
| DOIs | |
| Publication status | Published - 21 Aug 2026 |
Bibliographical note
Publisher Copyright:© 2026 The Authors
UN SDGs
This output contributes to the following UN Sustainable Development Goals (SDGs)
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SDG 3 Good Health and Well-being
Keywords
- CARC/CRAC
- Cancer
- Cell biology
- Human metabolism
- TMEM97
- cholesterol biosynthesis
- metabolic reprogramming
- mitochondrial bioenergetics
- oxidative phosphorylation
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