ArticleCytotechnology2025
Mechanism of lncRNA WARS2-IT1 promoting angiogenesis of glioma through miR-299-3P/VEGFA axis and activating PI3K/AKT signaling pathway.
Article in Cytotechnology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Sevoflurane is associated with reduced EGFR-VEGF-AKT signaling in glioma tissues relative to propofol: a bioinformatics and clinical pilot study.Frontiers in oncology · 2026Article
- XPNPEP2 regulates angiogenesis via modulation of mitochondrial function through SLC25A6.Frontiers in cell and developmental biology · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioma is a common primary intracranial tumor with easy recurrence and poor prognosis. Emerging evidence has highlighted the involvement of LncRNA in glioma proliferation, invasion, migration and angiogenesis, but at present, there is no relevant research on LncRNA WARS2-IT1. We performed qRT-PCR and Western blotting to evaluate the expression of related RNA in glioma. Cell Counting Kit-8, Scratch-healing test, Transwell, EDU test to assess the cell proliferation, migration and invasion ability in glioma and Tube formation assay contributed to endothelial cell angiogenesis. Apoptosis was measured via flow cytometry. Bioinformatics prediction and dual-luciferase reporter assays were conducted to validate the regulatory interactions in T98G and U251 cell lines. Results showed that lncRNA WARS2-IT1 and VEGFA were highly expressed in glioma cells, while miR-299-3p was enriched in normal glial HEB cells. WARS2-IT1 Knockdown significantly suppressed glioma cell proliferation, migration, invasion, and endothelial angiogenesis, while promoting apoptosis. Mechanistically, WARS2-IT1 harbored a complementary binding site for miR-299-3p, which directly targeted the 3-UTR of VEGFA. Further analysis revealed that WARS2-IT1 promotes glioma progression and angiogenesis through the PI3K/AKT signaling pathway. These findings suggest that the oncogenic lncRNA WARS2-IT1 contributes to glioma pathogenesis by upregulating VEGFA via sponging miR-299-3p, highlighting its therapeutic target potentiality. Supplementary Information: The online version contains supplementary material available at 10.1007/s10616-025-00824-5.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.