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Updated: Jan 13, 2026

Tumor Treating Field Therapy in Combination with Bevacizumab for the Treatment of Recurrent Glioblastoma
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Published on: October 27, 2014

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Reprogramming the Apoptosis-Autophagy Axis in Glioblastoma: The Central Role of the Bcl-2:Beclin-1 Complex and

Monika Christoff1, Amelia Szczepańska1, Joanna Jakubowicz-Gil2

  • 1Faculty of Biology and Biotechnology, Maria Curie-Skłodowska University, Akademicka 19, 20-033 Lublin, Poland.

Cells
|January 9, 2026
PubMed

Insights

Glioblastoma cells resist therapy by altering apoptosis and autophagy. Targeting the Bcl-2:beclin-1 complex can rebalance these cell death pathways, potentially overcoming glioblastoma resistance.

Area of Science:

  • Oncology
  • Cell Biology
  • Molecular Biology

Background:

  • Glioblastoma multiforme (GBM) displays significant therapeutic resistance.
  • This resistance is linked to the modulation of regulated cell death pathways, particularly apoptosis and autophagy.
  • The interplay between apoptosis and autophagy is critical in determining glioma cell fate under treatment stress.

Purpose of the Study:

  • To review the role of the Bcl-2:beclin-1 complex in controlling the apoptosis-autophagy axis in GBM.
  • To highlight how signaling networks regulate the balance between apoptosis and autophagy.
  • To explore therapeutic strategies targeting this crosstalk to overcome GBM drug resistance.

Main Methods:

  • Literature review focusing on molecular mechanisms of cell death in GBM.
  • Analysis of signaling pathways (PI3K/AKT/mTOR, Ras/Raf/MEK/ERK, PLCγ1/PKC) influencing the Bcl-2:beclin-1 complex.
  • Integration of concepts in cell death reprogramming and systems-level signaling.

Main Results:

  • The Bcl-2:beclin-1 complex acts as a key molecular switch governing glioma cell survival versus death.
  • Survival signaling pathways dynamically modulate the balance between apoptosis and autophagy.
  • Dysregulation of this balance contributes to glioblastoma's resistance to therapy.

Conclusions:

  • Modulating the apoptosis-autophagy crosstalk, particularly the Bcl-2:beclin-1 complex, can sensitize GBM to therapies.
  • Targeting this complex and its upstream regulators offers a promising strategy to overcome GBM's adaptive plasticity.
  • This approach may open new avenues for combination treatment strategies in glioblastoma.
Keywords:
Bcl-2:beclin-1 complexapoptosisautophagycancer cellglioblastoma multiformemolecular switchprogrammed cell death axissurvival pathways

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