Cancer Stem Cells in Glioblastoma: The Role of the mTOR Pathway

Monica C Mureb1, Sabrina L Zeller1, Haylen T Rosberger1

  • 1Department of Neurosurgery, New York Medical College/Westchester Medical Center, Valhalla, NY, U.S.A.

Anticancer Research
|June 27, 2025
PubMed

Insights

Glioblastoma stem cells (CSCs) drive tumor recurrence. Inhibiting the mechanistic target of rapamycin (mTOR) pathway, often dysregulated in glioblastoma due to PTEN loss, may offer a new therapeutic strategy against these resilient cancer stem cells.

Area of Science:

  • Neuro-oncology
  • Cancer Stem Cell Biology
  • Molecular Signaling Pathways

Background:

  • Glioblastoma is an aggressive brain tumor with poor prognosis, often recurring due to genetic abnormalities and cancer stem cells (CSCs).
  • CSCs contribute significantly to glioblastoma recurrence, growth, and invasion, making them critical therapeutic targets.
  • The mechanistic target of rapamycin (mTOR) pathway regulates cell proliferation and migration, and its aberrant activation is implicated in glioblastoma pathogenesis.

Purpose of the Study:

  • To explore the role of mTOR and associated signaling pathways in regulating glioblastoma stem cells.
  • To define the therapeutic potential of targeting mTOR signaling in glioblastoma treatment.

Main Methods:

  • Review of current literature on glioblastoma, cancer stem cells, and mTOR signaling.
  • Analysis of the molecular mechanisms linking PTEN loss, mTOR activation, and glioblastoma CSC behavior.

Main Results:

  • Loss of phosphatase and tensin homolog (PTEN) frequently occurs in glioblastoma, leading to mTOR pathway hyperactivation.
  • Aberrant mTOR signaling in glioblastoma CSCs promotes tumor growth, recurrence, and invasion.
  • Targeting the mTOR pathway presents a promising strategy to eliminate glioblastoma CSCs.

Conclusions:

  • The mTOR pathway is a critical regulator of glioblastoma stem cells.
  • Inhibition of mTOR signaling holds potential as a therapeutic approach for glioblastoma, specifically targeting CSCs to overcome treatment resistance and recurrence.

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