ArticleJournal of neuro-oncology2025
TMEM164 enhances radioresistance of GBM cells by inhibiting the FASN-NADPH-ROS axis.
Article in Journal of neuro-oncology, 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.
- Mechanism of ECM Stiffness-Integrin-Hippo-ABCG1 axis in regulating ferroptosis and targeted nanodrug intervention in LUAD.Respiratory research · 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
9 authors.
Funding
Abstract
purposeGlioblastoma multiforme (GBM), one of the most aggressive primary brain malignancies, remains a major therapeutic challenge in contemporary neuro-oncology. Radiotherapy, an essential component of current standard therapeutic protocol, still has persistently poor clinical efficacy in the intrinsic radioresistance of GBM. Therefore, elucidating the underlying mechanisms of radioresistance is critical for optimizing therapeutic outcomes in GBM patients.
methodsRadioresistant GBM cell lines U251R were established by irradiating U251 cells with fractionated dose of 60 Gy in total. RNA-seq and TMT assays were applied, combined with GEO, KEGG and other databases to analyze the role of TMEM164 in regulating the radiosensitivity of GBM cells. Pharmacological inhibition of cell death pathways was employed to identify the predominant cell death mechanism influencing TMEM164-mediated radioresistance in GBM cells. The intracellular levels of NADPH, lipid droplet and ROS were detected after radiation to assess the effect of TMEM164 on lipid metabolism. The effect of TMEM164 on necroptosis through FASN-NADPH-ROS axis was verified by rescue experiments.
resultsThrough bioinformatics analysis, TMEM164 was identified as a key gene regulating GBM cells' radiosensitivity. Knockdown of TMEM164 significantly increased necroptosis in U251R and T98G cells. Integrated enrichment analysis of RNA-seq and TMT data revealed that FASN interacted with TMEM164. Excessive NADPH consumption led to intracellular ROS accumulation, thereby increasing radiosensitivity in GBM cells.
conclusionsOur findings indicated that TMEM164 might serve as a critical biological target of GBM cells radioresistance, providing a novel theoretical basis for GBM radiotherapy.
Indexed as
Identifiers
40982109What 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.