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

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A. A. Khalil^1,2* and M. J. Jameson^1*

¹University of Virginia Health System, Division of Head and Neck Oncologic and Microvascular Surgery, Department of Otolaryngology, Head and Neck Surgery, 1215 Charlottesville, Virginia, USA; E-mail: mark.jameson@virginia.edu

²Menoufiya University, National Liver Institute, Department of Biochemistry, Egypt; E-mail: ashkalil2010@gmail.com

^* To whom correspondence should be addressed.

Received July 25, 2016; Revision received September 8, 2016

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Sodium orthovanadate (SOV) is a general inhibitor of tyrosine phosphatases, a large family of enzymes that catalyze the removal of phosphate groups from tyrosine residues. SOV is commonly used in the laboratory to preserve the protein tyrosyl phosphorylation state of proteins under study. It has shown promising antineoplastic activity in some human cancer cell lines; this effect has not been fully investigated in head and neck squamous cell carcinoma. In this study, the effect of SOV on cell growth, proliferation, viability, and apoptosis was assessed in Cal27 cells, an oral squamous cell carcinoma (OSCC) cell line. SOV exhibited dose-dependent inhibition of cell growth and decrease in cell viability and colony formation. The IC₅₀ values for treatment lasting 72 h and 7 days were 25 and 10 µM, respectively. The cytotoxic effect of the drug was associated with poly(ADP-ribose)polymerase cleavage detected by immunoblot. Flow cytometry of Cal27 cells stained with annexin V-FITC and propidium iodide showed a dose-dependent increase in apoptosis that reached approximately 40% at 25 µM SOV. These findings demonstrate that SOV has in vitro antiproliferative and proapoptotic effect on OSCC cells.

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KEY WORDS: sodium orthovanadate, oral cavity cancer, squamous cell carcinoma

DOI: 10.1134/S0006297917020067

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