alexa Vitamin C and K3 Combination Causes Enhanced Anticancer Activity against RT-4 Bladder Cancer Cells
ISSN: 1948-5956

Journal of Cancer Science & Therapy
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Research Article

Vitamin C and K3 Combination Causes Enhanced Anticancer Activity against RT-4 Bladder Cancer Cells

Karen McGuire1, James Jamison1*, Jacques Gilloteaux2 and Jack L. Summers1

1The Apatone Development Center, St. Thomas Hospital, Summa Health System, USA

2Department of Anatomical Sciences, St Georges’ University International School of Medicine, K B Taylor Scholar’s Programme, Newcastle upon Tyne, UK

*Corresponding Author:
James M. Jamison, Ph.D
Summa Health System Foundation
St. Thomas Hospital 444 N. Main Street, Akron, Ohio 44310, USA
Tel: (330) 379-8178
Fax: (330) 379-8177
E-mail: [email protected]

Received Date: August 19, 2013; Accepted Date: October 07, 2013; Published Date: October 09, 2013

Citation: McGuire K, Jamison J, Gilloteaux J, Summers JL (2013) Vitamin C and K3 Combination Causes Enhanced Anticancer Activity against RT-4 Bladder Cancer Cells. J Cancer Sci Ther 5:325-333. doi:10.4172/1948-5956.1000223

Copyright: © 2013 McGuire K, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

 

Abstract

Introduction: Vitamin C (VC), Vitamin K3 (VK3) and the combination (VC:VK3) were evaluated against human bladder cancer cell lines RT-4 and T24 to evaluate their synergistic anticancer activity.

Methods/Results: An MTT assay compared a 1hr pulsed versus a 5hr continuous exposure. VC:VK3 was synergistic, increasing the antitumor activity 12- to 24 fold for RT-4 cells. VC:VK3 pulsed versus continuous exposure produced comparable CD50 values, indicating a triggered response involving a catalase reversible redox mechanism generating hydrogen peroxide. Hydrogen peroxide production caused lipid peroxidation and depletion of cellular thiols. ATP levels were measured over 5hrs to determine metabolic effects where VC:VK3 caused a unique spike in ATP levels. Though the cause of the ATP spike is unknown a possible mechanism is a shunt formed around a defective region of complex III of the ETC from coenzyme Q to cytochrome c, producing a shift from glycolytic to oxidative metabolism and a diminution of lactic acidosis. Analysis of mitochondrial and extra mitochondrial calcium levels revealed a unique calcium pattern for RT4 cells treated with CD90 doses of VC, VK3 or VC:VK3.

Conclusion: VC:VK3 was able to cause autoschizic cell death through oxidative stress, thiol depletion, lipid peroxidation, modification of ATP levels and calcium regulation. Because of these results, VC:VK3 was granted orphan drug status for the treatment of metastatic or locally advanced, inoperable transitional cell carcinoma of the urothelium (stage III and IV bladder cancer). Efforts are underway to conduct a phase II clinical trial for this indication.

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