ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026
The Tumor-to-Endothelial Transfer of FTO Promotes Vascular Remodeling and Metastasis in Nasopharyngeal Carcinoma.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- FTO-modulated mJournal of translational medicine · 2026Article
- The Tumor-to-Endothelial Transfer of FTO Promotes Vascular Remodeling and Metastasis in Nasopharyngeal Carcinoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Reader-dependent functional duality of FTO: a context-switching node at the intersection of immune evasion and therapeutic resistance.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
24 authors.
Funding
Abstract
Cancer stem-like cells (CSCs) in nasopharyngeal carcinoma (NPC) exhibit heightened stemness, invasiveness, and resistance to therapy, posing significant challenges for diagnosis and treatment. How CSCs interact with the endothelium to drive vascular remodeling and metastasis remains unclear. Using spatially resolved multi-omic profiling of clinical NPC samples and experimental validation, a tumor-endothelial crosstalk mechanism is identified, driven by the NOTCH1-FTO-SPARC axis. Omics analysis reveals a distinct NOTCH1⁺ CSC subpopulation with enhanced tumorigenic potential. FTO, a direct transcriptional target and key effector of NOTCH1, promotes vascular remodeling and metastasis. Notably, NOTCH1⁺ tumors secreted FTO via exosomes, which are readily taken up by endothelial cells. Within recipient endothelial cells, accumulated FTO disrupts endothelial tight junctions by suppressing YTHDF2-mediated m6A modification, stabilizing SPARC mRNA, and increasing SPARC protein levels. Inhibition of FTO with DAC51 significantly suppresses metastasis in NPC mouse models. Clinically, metastatic NPC patients show elevated levels of NOTCH1⁺ CSC-CTCs (EPCAM⁺ EBNA1⁺ NOTCH1⁺ CD45
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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.