ReviewCells2025
Reprogramming the Apoptosis-Autophagy Axis in Glioblastoma: The Central Role of the Bcl-2:Beclin-1 Complex and Survival Signalling Networks.
Review in Cells, 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.
- Brazilin induces apoptosis and autophagy in human glioblastoma cells via the PI3K/AKT/mTOR signaling pathway.American journal of translational research · 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
4 authors.
Funding
Abstract
Glioblastoma multiforme (GBM) exhibits remarkable resistance to therapy, mainly due to its capacity to modulate regulated cell death pathways. Among these, apoptosis and autophagy are dynamically interconnected, determining cell fate under therapeutic stress. The interaction between beclin-1 and Bcl-2 proteins may represent a key molecular switch that controls whether glioma cells undergo survival or death. This review highlights the crucial role of the Bcl-2:beclin-1 complex in controlling apoptosis-autophagy axis in GBM, emphasising how survival signalling networks, including PI3K/AKT/mTOR, Ras/Raf/MEK/ERK, and PLCγ1/PKC pathways regulated by the TrkB receptor, modulate this balance. We summarise recent insights into how these pathways coordinate the shift between apoptosis and autophagy in glioma cells, contributing to drug resistance. Furthermore, we highlight how modulating this crosstalk can sensitise GBM to conventional and emerging therapies. Integrating new concepts of cell death reprogramming and systems-level signalling analysis, we propose that targeting the Bcl-2:beclin-1 complex and its upstream regulators could overcome the adaptive plasticity of glioblastoma multiforme and open new directions for combination treatment strategies.
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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.