Necrotic and apoptotic adipocytes in the hypoxic tumor microenvironment supply triglycerides to induce cisplatin resistance in the metastatic lymph nodes of head and neck carcinoma
Li F., Huang H., Huang Q., Mao X., Cong N., Zhuang W.
Prospective Study, published in Cell Death Dis (2025) — summary generated from the PubMed abstract.
Early human evidence such as case series or small samples is exploring possible benefits.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Prospective Study
- Journal
- Cell Death Dis (2025)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 41285714
- PMCID
- PMC12644729
- DOI
- 10.1038/s41419-025-08239-y
Abstract (original English)
Metastatic lesions in cervical lymph nodes are generally less sensitive to induction chemotherapy than primary tumors, making cervical lymph node metastasis one of the most significant prognostic factors in head and neck squamous cell carcinoma (HNSCC). However, the underlying mechanism of cisplatin resistance in these lymph nodes remains unclear. Lipidomic analysis of 21 HNSCC patients revealed distinct lipid profiles between cervical lymph node metastases and primary tumors, with triglycerides notably enriched in the metastatic nodes, suggesting a critical role for adipocytes. Further investigation confirmed the presence of cancer-associated adipocytes within cervical lymph node metastases, which supply triglycerides to tumor cells. The hypoxic tumor microenvironment promotes apoptosis and necrosis in adipocytes, a process accelerated by hypoxic tumor cells, leading to increased triglyceride release. In HNSCC cells, triglycerides promote lipid droplet accumulation and enhance contact between lipid droplets and mitochondria via the interaction of perilipin-2 (PLIN2) and carnitine palmitoyltransferase-1A (CPT1A), thereby reversing cisplatin-induced rises in intracellular reactive oxygen species (ROS). In vivo, xenograft tumors located in adipocyte-rich regions showed larger volume and greater mass after cisplatin treatment. This study is the first to demonstrate that adipocytes
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
Evidence level
Early human evidence such as case series or small samples is exploring possible benefits.
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