ArticleCancer letters2025
The role of 7-dehydrocholesterol in inducing ER stress and apoptosis of head and neck squamous cell carcinoma.
Article in Cancer letters, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed.
- DHCR24 promotes endometrial carcinoma progression and is associated with cellular senescence regulation.Medical oncology (Northwood, London, England) · 2026Article
- Compartmentalization of DHCR7 links 7-DHC metabolism to B-ring unsaturated steroid synthesis in the equine fetal gonad.Endocrinology · 2026Article
- The Natural Triterpenoid Alisol B Overcomes Temozolomide Resistance in Glioblastoma Through Multi-Target Mechanisms: Coordinated Epigenetic, Metabolic, and Cell-Cycle Reprogramming.International journal of molecular sciences · 2026Article
- 7-Dehydrocholesterol attenuates osteoarthritis by synergistically inhibiting oxidative stress, inflammation, and ferroptosis in macrophages.Frontiers in pharmacology · 2026Article
- Interpretable Multi-Cancer Early Detection Using SHAP-Based Machine Learning on Tumor-Educated Platelet RNA.Diagnostics (Basel, Switzerland) · 2025Article
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Authors and funding
19 authors.
Funding
Abstract
Alterations of metabolic pathways that sustain cancer cell survival often offer promising therapeutic avenues. Here, we show that enhanced de novo cholesterol biosynthesis is crucial for the survival of head and neck squamous cell carcinoma (HNSCC). Transcriptomic analysis of HNSCC tissues identified profound dysregulation in steroid and cholesterol metabolism compared to normal tissues. Inhibition of two key enzymes, DHCR7 and DHCR24, which mediate cholesterol biosynthesis, induced apoptosis in HNSCC cells, even when cholesterol levels were restored. Metabolomic profiling revealed the accumulation of 7-dehydrocholesterol (7-DHC) upon DHCR7 or DHCR24 inhibition, triggering endoplasmic reticulum (ER) stress and promoting further cell death. These findings suggest that HNSCC cells adapt to ER stress by modulating 7-DHC levels through enhancing DHCR7 and DHCR24 levels, highlighting a metabolic vulnerability in HNSCC and demonstrating a direct link between cholesterol metabolism and ER stress in cancer cell viability.
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Registered trials
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