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ISSN: 2165-7092

Pancreatic Disorders & Therapy
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Research Article

Ascorbate-Induced Autophagy in Pancreatic Cancer

Jessemae L Welsh1, Juan Du2, Zita A Sibenaller1, Sean M Martin2, C Michael Knudson3,4 and Joseph J Cullen1,2,4,5*
1Department of Surgery, University of Iowa Carver College of Medicine, Iowa City, IA, USA
2Radiation Oncology, University of Iowa Carver College of Medicine, Iowa City, IA, USA
3Pathology, University of Iowa Carver College of Medicine, Iowa City, IA, USA
4Holden Comprehensive Cancer Center, Iowa City, IA, USA
5Veterans Affairs Medical Center, Iowa City, IA, USA
Corresponding Author : Joseph J Cullen
1528 JCP, University of Iowa Hospitals and Clinics
Iowa City, IA 52242, USA
Tel: (319) 353-8297
Fax: (319) 356-8378
E-mail: [email protected]
Received May 07, 2013; Accepted June 26, 2013; Published June 28, 2013
Citation: Welsh JL, Du J, Sibenaller ZA, Martin SM, Knudson CM, et al. (2013) Ascorbate-Induced Autophagy in Pancreatic Cancer. Pancreatic Dis Ther 3:119. doi:10.4172/2165-7092.1000119
Copyright: © 2013 Welsh JL, 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

Pharmacological ascorbate induces autophagy in pancreatic cancer, which is characterized by accumulation of autophagosomes and the processing of microtubule-associated protein light chain 3 (LC3) to the lipidated form, LC3- II. Prior studies have demonstrated LC3-II upregulation in pancreatic cancer cells after gemcitabine chemotherapy or ionizing radiation. The aim of this study was to determine the role of autophagy in pharmacological ascorbate-induced cytotoxicity. Pancreatic cancer cells were generated to stably overexpressLC3 fused to a green fluorescent protein (MIA PaCa-2 LC3-GFP). MIA PaCa-2 LC3-GFP cells had a higher LC3-II/LC3-I ratio at 6 and 24 hours and demonstrated a clonogenic survival advantage after pharmacological ascorbate treatment compared to parental cells. In cells with knockdown of Atg5, there was increased susceptibility to pharmacological ascorbate-induced cytotoxicity. Our data indicate autophagy may be an important survival mechanism after pharmacological ascorbate-induced cytotoxicity, while impairment of autophagy can re-sensitize cells to ascorbate. LC3 over expression has a protective effect on cell survival after ascorbate treatment. Autophagy-modulating drugs may be an important adjunct for enhancement of ascorbate-induced cytotoxicity as well as a potential therapy for re-sensitization of chemoradiation-resistant tumors.

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