ArticleJournal for immunotherapy of cancer2025
Aberrant lipid metabolism reshapes the immune landscape in bone metastasis of nasopharyngeal carcinoma.
Article in Journal for immunotherapy of cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- PGE2-mediated NK cell reprogramming drives acquired immunotherapy resistance in lung adenocarcinoma.Journal for immunotherapy of cancer · 2026Article
- Breaking the immune "cold niche" in bone metastasis: core mechanisms of the multidimensional interwoven regulatory network and precision breakthrough strategies.Molecular cancer · 2026Review
- Targeting regulatory T cells in gastrointestinal cancers: current status and future perspectives.International journal of clinical oncology · 2026Review
- The emerging role of SPHK1 at the immune-metabolic interface: a pan-cancer integrative analysis.Scientific reports · 2026Article
- Overcoming barriers in CAR-NK immunotherapy: CRISPR-Driven advances in checkpoint editing and allogeneic design.Functional & integrative genomics · 2025Review
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Authors and funding
10 authors.
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Abstract
backgroundBone metastasis (BM) drives therapeutic resistance and mortality in nasopharyngeal carcinoma (NPC). Tumor metabolites are crucial for NPC metastasis; however, the mechanisms by which these metabolites synergistically alter the immune microenvironment to promote BM remain unclear.
methodsIn this study, limited immune infiltration was observed in the NPC BM tumor microenvironment. Multiomics analysis has identified sphingosine kinase 1 (SPHK1) as a pivotal mediator driving BM and immune evasion in NPC, orchestrating the production of 1-phosphorylated sphingosine (S1P), which is critical for NPC pathogenesis.
resultsThe aberrant buildup of lipid metabolites, along with immune microenvironment shifts, serves as a critical driver of NPC BM. Mechanistically, S1P enhanced osteoclast recruitment via S1PR3 binding and activated the Hippo pathway, worsening bone colonization and facilitating immune evasion by expanding the exhausted CD8
conclusionsThe synergy between the SPHK1 inhibitor PF543 and anti-programmed cell death protein 1 therapy amplified treatment effectiveness beyond standalone approaches. Overall, the SPHK1/S1P pathway advances NPC growth and aids in suppressing immune defense. Regulation of lipid metabolism may be a therapeutic target against BM in NPC and may improve the effectiveness of immunotherapy.
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