ArticleScientific reports2025
Rubidium ions as a novel therapeutic approach for glioblastoma.
Article in Scientific reports, 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
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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.
- Rubidium chloride induces ferroptosis in glioblastoma cells by disrupting glutathione metabolism and redox homeostasis.Cancer cell international · 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
8 authors.
Funding
Abstract
Glioblastoma (GBM) is a highly aggressive brain tumor with limited treatment options, mainly due to challenges such as incomplete resection and blood-brain barrier limitations. Rubidium, a naturally occurring alkali metal with favorable biocompatibility, widely used in myocardial and tumor perfusion imaging as a blood flow tracer, is repurposed in this study to investigate its potential therapeutic effects and mechanisms against GBM. The impacts of rubidium ions (Rb⁺) on GBM cells were assessed through functional assays evaluating proliferation, migration, invasion, and apoptosis. RNA sequencing and Western blot analyses were employed to investigate molecular mechanisms, while in vivo models were used to evaluate therapeutic efficacy and safety. Rb⁺ treatment significantly suppressed GBM cell proliferation, migration, and invasion, while inducing apoptosis and cell cycle arrest at the G2/M phase. Mechanistic studies revealed that Rb⁺ downregulated the phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) pathway, contributing to the induction of apoptosis in tumor cells. In vivo, Rb⁺ exhibited potent anti-tumor activity with no detectable adverse effects on major organs, physiological functions, or behavior in mice. Our findings highlight Rb⁺ as a promising and innovative candidate for GBM therapy, leveraging the PI3K/AKT/mTOR pathway to inhibit tumor growth and promote apoptosis. This study underscores the potential of Rb⁺ in addressing the urgent need for novel GBM treatments, warranting further preclinical and clinical investigations.
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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 OpenQuestion graph.