The difference of sensitivity between BXPC-3 and K562 cells by treatments with combination of indole-3-acetic acid and horseradish peroxidase

Abstract

The difference of sensitivity to indole-3-acetic acid (IAA) combined with horseradish peroxidase (HRP) in K562 and BXPC-3 cells was investigated. The cell proliferation was determined by MTT assay. The cell cycle and apoptosis of K562 and BXPC-3 cells were examined by a fluorescence flow cytometer (FCM) and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) respectively. The experimental results show that IAA and HRP could inhibit BXPC-3 cell proliferation greatly compared with K562 cell during the first 48 h. The cell cycle was arrested predominantly at G2/M phase in K562 and BXPC-3 cells. The cell apoptosis of K562 and BXPC-3 was induced by IAA/HRP. There was a significant difference between the two cell lines since BXPC-3 cells were more sensitive than K562 cells by treatments with combination of IAA and HRP.

Keywords

indole-3-acetic acids / horseradish peroxidase / BXPC-3 cell / K562 cell / apoptosis

References

[1] Folkes LK, Wardman P. Oxidative Activation of Indole-3-acetic Acids to Cytotoxic Species—A Potencial New Role for Plant Auxins in Cancer Therapy[J]. J. Biochemical Pharmacology, 2001, 61: 129-136.

[2] Greco O, Rossiter S, Kanthou C, . Horseradishperoxidase-mediated Gene Therapy Choice of Prodrugs in Oxic and Anoxic Tumor Conditions [J]. J. Molecular Cancer Therapeutics, 2001, 1: 151-160.

[3] Folkes LK, Greco O, Dachs GO, . 5-Fluoroindole-3-acetic Acid: A Prodrug Activated by a Peroxidase with Potential for Use in Targeted Therapy [J]. Biochemical Pharmscology, 2002, 63: 265-272.

[4] Rossiter S, Folkes LK, Wardman P. Halogenated Indole-3-acetic Acids as Oxidatively Activated Prodrugs with Potential for Targeted Cancer Therapy [J]. Bioorganic & Medicinal Chemistry Letters, 2002, 12: 2523-2526.

[5] Folkes LK, Dennis MF, Stratford MR, . Peroxidase-catalyzed Effects of Indole-3-acetic Acid and Analogues on Lipid Membranes, DNA and Mammalian Cells in vitro [J]. J. Biochemical Pharmacology, 1999, 57: 375-382.

[6] Folkes LK, Candeias LP, Wardman P, . Toward Targeted “Oxidation Therapy” of Cancer: Peroxidase-catalyzed Cytotoxicity of Indole-3-acetic Acids [J]. J. Radiation Oncology Biol. Phys., 1998, 42: 917-920.

[7] Wardman P. Indole-3-acetic Acid and Horseradish Peroxidase; a New Prodrug/Enzyme Combination for Targeted Cancer Therapy [J]. J. Curr. Pharm Des., 2002, 8: 1363-1374.

[8] Makin G, Dive C. Recent Advances in Understanding Apoptosis: New Therapeutic Opportunities in Cancer Chemotherapy [J]. J. Trends Mol. Med., 2003, 9: 251-255.

[9] Greco O, Dachs GU, Tozer GM, . Mechanisms of Cytotoxicity Induced by Horseradish Peroxidase/Indole-3-acetic Acid Gene Therapy[J]. J. J Cell Biochem., 2002, 87: 221-232.

[10] Kima DS, Jeonb SE, Park KC. Oxidation of indole-3-acetic Acid by Horseradish Peroxidase Induces Apoptosis in G361 Human Melanoma Cells[J]. J. Cellular Signalling, 2004, 16: 81-88.

[11] De Melo MP, Pithon-Curi TC, Curi R. Indole-3-acetic Acid Increases Glutamine Utilization by High Peroxidase Activity-presenting Leukocytes[J]. J. Life Science, 2004, 75: 1713-1725.

[12] De Melo MP, De Lima TM, Pithon-Curi TC, . The Mechanism of Indole Acetic Acid Cytotoxicity[J]. J. Toxicology Letters, 2004, 148: 103-11.

[13] Pietenpol JA, Stewart ZA. Cell Cycle Checkpoint Signaling: Cell Cycle verus Apoptosis[J]. J. Toxicology, 2002, 181–182: 475-481.

[14] Kim JY, Kim CH, Stratford IJ, . The Bioreductive Agent RH1 and Irradiation both Cause G2/M Cell Cycle Phase Arrest and Polyploidy in a p53-mutated Human Breast Cancer Cell Line[J]. J. Radiation Oncology Biol. Phys., 2004, 58: 376-385.

[15] Armstrong JS, Hornung B, Lecane P, . Rotenone-induced G2/M Cell Cycle Arrest and Apoptosis in a Human B Lymphoma Cell Line PW[J]. J. Biochemical and Biophysical Research Communications, 2001, 289(5): 973-978.