AnvirzelTMregulates cell death through inhibiting GSK-3 activity in human U87 glioma cells

Sule Terzioglu-Usak1, Arife Nalli2, Birsen Elibol1

  • 1Department of Medical Biology, Bezmialem Vakif University Medical School, Istanbul, Turkey.

Neurological Research
|January 5, 2020
PubMed

Insights

Anvirzel™, a cardiac glycoside mixture, effectively inhibited U87 glioblastoma cell growth. It modulated cell death pathways by inhibiting GSK-3, NOS, and HIF1-α while activating ERK.

Area of Science:

  • Oncology
  • Pharmacology
  • Molecular Biology

Background:

  • Cardiac glycosides show anti-cancer potential by inhibiting cancer cell proliferation and inducing apoptosis or autophagy.
  • Anvirzel™ contains oleandrin and oleandrigenin, two toxic cardiac glycosides with potential anti-cancer applications.

Purpose of the Study:

  • To investigate the signaling pathways involved in the differential cell death induced by Anvirzel™ in U87 human glioblastoma cells.
  • To assess the anti-proliferative and anti-migratory effects of Anvirzel™ on U87 cells.

Main Methods:

  • U87 cells were treated with varying doses of Anvirzel™ (10-250 μg/ml).
  • Cell proliferation was measured using the WST-1 assay.
  • Cell migration was assessed via wound healing assay.
  • Protein expression related to cell death was analyzed using Western blot.

Main Results:

  • Anvirzel™ significantly inhibited U87 cell growth in a time- and dose-dependent manner (24h and 48h treatments).
  • Anvirzel™ treatment led to the inhibition of GSK-3, NOS, and HIF1-α protein expressions.
  • Anvirzel™ treatment resulted in the activation of ERK signaling pathway in U87 cells.

Conclusions:

  • Anvirzel™ exhibits anti-proliferative and anti-migratory effects on U87 glioblastoma cells.
  • The compound appears to regulate cell death through mechanisms distinct from classical apoptosis.
  • Further research is needed to fully elucidate the mechanistic insights into Anvirzel™'s cell death signaling pathways.

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