Sodium orthovanadate inhibits proliferation and triggers apoptosis in oral squamous cell carcinoma in vitro

被引:0
作者
A. A. Khalil
M. J. Jameson
机构
[1] University of Virginia Health System,Department of Otolaryngology, Head and Neck Surgery
[2] Division of Head and Neck Oncologic and Microvascular Surgery,National Liver Institute, Department of Biochemistry
[3] Menoufiya University,undefined
来源
Biochemistry (Moscow) | 2017年 / 82卷
关键词
sodium orthovanadate; oral cavity cancer; squamous cell carcinoma;
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中图分类号
学科分类号
摘要
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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页码:149 / 155
页数:6
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  • [1] Alonso A.(2004)Protein tyrosine phosphatases in the human genome Cell 117 699-711
  • [2] Sasin J.(2008)Cysteine S-nitrosylation protects protein-tyrosine phosphatase 1B against oxidation-induced permanent inactivation J. Biol. Chem. 283 35265-35272
  • [3] Bottini N.(2000)Phosphatase inhibition promotes antiapoptotic but not proliferative signaling pathways in erythropoietin-dependent HCD57 cells Blood 96 2084-2092
  • [4] Friedberg I.(1999)Sodium vanadate inhibits apoptosis in malignant glioma cells: a role for Akt/PKB J. Biomed. Sci. 6 213-218
  • [5] Friedberg I.(2001)Vanadate facilitates interferon alpha-mediated apoptosis that is dependent on the Jak/Stat pathway J. Biol. Chem. 276 13547-13553
  • [6] Osterman A.(1997)Orthovanadate induces cell death in rat dentate gyrus primary culture Neuroreport 8 2465-2470
  • [7] Godzik A.(2011)ATM-dependent ERK signaling via AKT in response to DNA double-strand breaks Cell Cycle 10 481491-1149
  • [8] Hunter T.(1997)Role of oxidative stress in the action of vanadium phosphotyrosine phosphatase inhibitors. Redox independent activation of NF-kappaB J. Biol. Chem. 272 11541-132
  • [9] Dixon J.(2000)Poly(ADP-ribosyl)ation genomic instability, and longevity, Ann. NY Acad. Sci. 908 126-5
  • [10] Mustelin T.(2001)Poly(APD-ribosyl)ation a DNA damage-driven protein modification and regulator of genomic instability, Cancer Lett. 163 1-2134