ArticleCancer & metabolism2025
Improved VPS4B O-GlcNAc modification triggers lipid droplets transferring from adipocytes to nasopharyngeal carcinoma cells.
Article in Cancer & metabolism, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Toll-like receptor 4 signaling links cytoskeletal remodeling to lipid accumulation in macrophages.Inflammation and regeneration · 2026Review
- Targeting metabolic reprogramming to enhance adoptive immunotherapy: emerging mechanisms and translational perspectives.Journal of translational medicine · 2026Review
- O-GlcNAcylation at the tumor-immune interface: a metabolic post-translational code driving immune evasion and therapy resistance in cancer.Frontiers in immunology · 2026Review
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Authors and funding
12 authors.
Funding
Abstract
backgroundThe tumor microenvironment (TME) supplies critical metabolites that support cancer cell survival and progression. Adipocytes support tumor progression by secreting free fatty acids (FFAs) and adipokines; however, the role and mechanisms underlying lipid droplet (LD) release from adipocytes remain elusive.
methodsUsing two nasopharyngeal carcinoma (NPC) cell lines and primary human pre-adipocytes (HPA), we evaluate the effect of LDs on cell growth, proliferation, colony formation, and migration. We also assess the roles of LD on the tumor progression in vivo. Using RNA-seq analysis, we elucidate the effect of hypoxic NPC cell-derived exosomes (H-exo) on the gene expression profile of adipocytes. By co-culture system, we investigated the effect of vacuolar protein sorting 4 homolog B (VPS4B)-annexin A5 (ANXA5) interaction on adipocyte LD maturity and release.
resultsHerein, we report that LDs, rather than FFAs, are the primary lipid form transferred from adipocytes to NPC cells, enhancing cancer progression. NPC cells internalize LDs directly via macropinocytosis, while H-exo induces oxidative stress and membrane fluidity in adipocytes, leading to LD release. Transcriptomic and proteomic analyses reveal that VPS4B triggers LD release by interacting with ANXA5, and low LKB1 in H-exo enhances VPS4B O-linked N-acetylglucosamine (O-GlcNAc) modification through the inhibition of serine/threonine kinase 11 (STK11/LKB1)-AMP-activated protein kinase (AMPK) pathway and activation of the hexosamine biosynthesis pathway (HBP) flux.
conclusionsThis study uncovers critical mechanisms of LD transfer in the TME, suggesting new therapeutic avenues in NPC.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.