ArticleCNS neuroscience & therapeutics2025
NONHSAT141192.2 Facilitates the Stemness and Radioresistance of Glioma Stem Cells via the Regulation of PIK3R3 and SOX2.
Article in CNS neuroscience & therapeutics, 2025. 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.
- Research progress on glioma drug resistance: mechanism analysis and therapeutic strategies.Frontiers in pharmacology · 2026Review
- Single-Cell Multiomic Profiling Uncovers Radiation Dosage-Sensitive, Cluster-Specific Regulatory Dynamics in Glioblastoma.bioRxiv : the preprint server for biology · 2025Article
- Epigenetic crosstalk between stem cells and tumors: mechanisms and emerging perspectives.American journal of stem cells · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors.
Funding
Abstract
backgroundGlioma stem cells (GSCs) contribute to the initiation, recurrence, metastasis, and drug resistance of glioblastoma multiforme (GBM). Long noncoding RNAs (lncRNAs) are critical modulators in the development and progression of GBM; however, specific lncRNAs related to GSCs remain largely unexplored. This study aims to identify dysregulated lncRNAs in GSCs, unravel their contributions to GBM progression, and propose new targets for diagnosis and treatment.
methodsGeneChip analysis was utilized to identify lncRNAs in GSCs. The expression of RNAs was examined using quantitative real-time PCR. Cell Counting Kit-8, tmorsphere formation assay, limiting dilution assay, apoptosis detection and intracranial xenograft models were performed to assess the stemness and radioresistance of GSCs. Transcriptomics analysis, RNA immunoprecipitation and dual-luciferase experiments were conducted for mechanistic studies.
resultsNONHSAT141192.2 exhibited elevated expression levels in aggressive GBM tissues compared to lower-grade gliomas. Silencing NONHSAT141192.2 resulted in a considerable decrease in GSC proliferation, tumor sphere formation, self-renewal and the expression of key stem cell markers. Furthermore, depletion of NONHSAT141192.2 enhanced GSC sensitivity to radiation, indicated by diminished viability and tumorsphere formation, increased cell apoptosis, and decreased tumor growth in intracranial xenograft models. Mechanistically, NONHSAT141192.2 upregulates the expression of SOX2 and PIK3R3 by sponging miR-4279, influencing GSC characteristics and their resistance to radiation.
conclusionThe study highlights a significant relationship between NONHSAT141192.2, GSC stemness, and radioresistance, emphasizing its potential as a therapeutic target for GBM treatment and radiosensitization.
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.