ArticleOncogene2025
sEV-mediated intercellular transformation from MGAT4A
Article in Oncogene, 2025. 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.
- LncRNA SBF2-AS1 Regulates Pyroptosis to PromoteMicroorganisms · 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
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
ncRNAs encapsulated in small extracellular vesicles (sEVs) facilitate intercellular communication and are associated with tumor progression. lncRNA-HOTAIRM1 is aberrantly expressed in various cancers. However, HOTAIRM1 expression and its downstream ceRNA network in CTCL remains unclear. In this study, we found that HOTAIRM1 was reduced in CTCL. Elevated HOTAIRM1 inhibited proliferation and induced apoptosis in vitro, resulting in reduced in vivo tumorigenic capacity. Whole-transcriptome sequencing and scRNA-Seq confirmed that differential expression of HOTAIRM1/miR-196b-5p/MGAT4A axis induces apoptosis resistance in CTCL. Mechanistically, reduced MGAT4A expression in CTCL leads to decreased N-glycosylation modification of membrane proteins and reduced Galectin-1 affinity, thereby inducing partial resistance to Galectin-1-induced apoptosis. Meanwhile, benign CD4 + T cells show sensitivity to Galectin-1-induced apoptosis due to their relatively higher MGAT4A expression. Furthermore, MGAT4A
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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.