ArticleBMC cancer2026
Multi-omics profiling reveals sphingolipid metabolism reprogramming of tumor-conditioned MDSCs in cervical cancer.
Article in BMC cancer, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- KRAS-mutated endometrial carcinomas: a comprehensive analysis of clinicopathological and molecular profiles across histological subtypes.Virchows Archiv : an international journal of pathology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors.
Funding
Abstract
backgroundMyeloid-derived suppressor cells (MDSCs) play a crucial role in the tumor microenvironment (TME) of cervical cancer (CC), yet the mechanisms underlying their reprogramming remain poorly understood.
methodsTo explore the immune microenvironment change in CC, we applied TCGA-CC immune microenvironment infiltration estimation analysis via Timer 2.0 online datasets. To generate tumor-conditioned MDSCs, the culture medium of MDSCs was supplemented with supernatants from the murine CC cell lines U14 and TC1, respectively. CCK8 assays, transwell migration experiments and qPCR were executed to test the proliferation, migration and iNOS expression. We then conducted proteomics and metabolomics analyses of tumor-conditioned MDSCs.
resultsThe tumor immune microenvironment analysis identified MDSCs as key components, predicting poor prognosis in CC. Tumor-conditioned MDSCs presented higher proliferation, migration and iNOS expression. Proteomics and metabolomics analyses showed significant changes in lipid metabolism, especially sphingolipid metabolism. Specifically, the Kng1-sphingosine 1-phosphate axis was identified as a central protein-metabolite regulatory node. Gain- and loss-of-function experiments confirmed that KNG1 modulates multiple cellular processes including proliferation, migration, iNOS expression, and sphingosine 1-phosphate production.
conclusionOur findings uncover sphingolipid metabolic reprogramming as a key mechanism in MDSCs-mediated immune suppression, and propose the Kng1-sphingosine 1-phosphate network as a potential therapeutic target for CC treatment.
Indexed as
Identifiers
What Socratic holds
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.