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Sodium Orthovanadate Inhibits Proliferation and Triggers Apoptosis in Oral Squamous Cell Carcinoma in vitro

A A Khalil1, M J Jameson

  • 1University of Virginia Health System, Division of Head and Neck Oncologic and Microvascular Surgery, Department of Otolaryngology, Head and Neck Surgery, Virginia, USA. mark.jameson@virginia.edu.

Biochemistry. Biokhimiia
|March 22, 2017
PubMed

Insights

Sodium orthovanadate (SOV) inhibits oral squamous cell carcinoma (OSCC) growth and viability. This tyrosine phosphatase inhibitor induces apoptosis in OSCC cells, suggesting potential as an anti-cancer therapeutic.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Oncology

Background:

  • Sodium orthovanadate (SOV) is a tyrosine phosphatase inhibitor.
  • SOV is used to maintain protein phosphorylation states.
  • Its antineoplastic activity in head and neck squamous cell carcinoma (HNSCC) is understudied.

Purpose of the Study:

  • To investigate the effect of SOV on oral squamous cell carcinoma (OSCC) cell line Cal27.
  • To assess SOV's impact on cell growth, proliferation, viability, and apoptosis.

Main Methods:

  • Cal27 cells were treated with varying SOV concentrations.
  • Cell growth, viability, and colony formation were measured.
  • Apoptosis was assessed using Annexin V-FITC and propidium iodide staining via flow cytometry.
  • Poly(ADP-ribose)polymerase cleavage was detected by immunoblot.

Main Results:

  • SOV demonstrated dose-dependent inhibition of cell growth, viability, and colony formation.
  • IC50 values were 25 µM (72h) and 10 µM (7 days).
  • SOV induced a dose-dependent increase in apoptosis, reaching ~40% at 25 µM.
  • Cytotoxicity correlated with poly(ADP-ribose)polymerase cleavage.

Conclusions:

  • SOV exhibits significant in vitro antiproliferative effects on OSCC cells.
  • SOV promotes apoptosis in OSCC cells.
  • These findings support SOV's potential as a therapeutic agent for OSCC.

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