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M2 receptor activation inhibits cell cycle progression and survival in human glioblastoma cells

Michela Ferretti1, Cinzia Fabbiano, Maria Di Bari

  • 1Department of Biology and Biotechnologies Charles Darwin, Research Centre of Neurobiology Daniel Bovet, La Sapienza, University of Rome, P.le Aldo Moro, 5-00185 Roma, Italy.

Journal of Cellular and Molecular Medicine
|March 16, 2013
PubMed

Insights

M2 muscarinic receptors are present in glioblastoma. Activating these receptors with arecaidine inhibits glioma cell growth and survival, suggesting a new therapeutic target for glioblastoma treatment.

Area of Science:

  • Neuro-oncology
  • Molecular biology
  • Pharmacology

Background:

  • Muscarinic receptors are implicated in tumor growth and propagation.
  • M2 muscarinic receptors are expressed in glioblastoma specimens and cell lines.

Purpose of the Study:

  • To investigate the role of M2 muscarinic receptors in glioblastoma.
  • To characterize the effects of the M2 agonist arecaidine on glioblastoma cell growth and survival.

Main Methods:

  • Cell growth and viability assays on glioblastoma cell lines (U251MG, U87MG) and primary cultures.
  • Flow cytometry (FACS) analysis for cell cycle assessment.
  • Chemosensitivity assays comparing arecaidine and temozolomide.

Main Results:

  • Arecaidine significantly decreased glioblastoma cell proliferation in a dose- and time-dependent manner.
  • Arecaidine induced cell cycle arrest at G1/S and G2/M phases.
  • Arecaidine promoted apoptosis and demonstrated comparable efficacy to temozolomide in glioma cell lines.

Conclusions:

  • M2 receptor activation inhibits glioma cell growth and survival.
  • M2 receptors represent a potential therapeutic target for glioblastoma treatment.

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