ReviewBiomedical reports2026
Decoding the S1P-S1PR axis in cancer: Mechanisms, pathways and therapeutic horizons (Review).
Review in Biomedical reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sphingosine-1-phosphate (S1P) and its five G protein-coupled receptors (S1PR1-S1PR5) regulate a broad range of processes that shape cancer progression, including proliferation, survival, angiogenesis, immune evasion and metastatic dissemination. Under physiological conditions, this signaling axis contributes to vascular integrity, immune cell trafficking and tissue homeostasis. In cancer, however, its output is not solely determined by ligand abundances. Rather, tumors reprogram the S1P-S1PR axis at a number of levels, coupling altered S1P production with receptor-specific changes in expression, localization and the signaling state to generate context-dependent malignant phenotypes. The present review provided a receptor-resolved synthesis of S1PR functions in cancer and examined the mechanisms that underlie pathway dysregulation, including transcriptional activation, epigenetic remodeling, microRNA loss, post-translational modifications and altered receptor trafficking and compartmentalization. It further discussed how metabolic amplification of S1P availability cooperates with receptor-level rewiring to sustain tumor progression, microenvironmental remodeling and therapeutic resistance. This framework positions the S1P-S1PR axis as a dynamically reprogrammed signaling network and highlights therapeutic strategies that concurrently target S1P production and receptor-mediated signaling as promising avenues for more-precise, biomarker-informed cancer treatment.
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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.