Oncotarget

Research Papers:

Induction of cellular prion protein (PrPc) under hypoxia inhibits apoptosis caused by TRAIL treatment

Jin-Young Park _, Jae-Kyo Jeong, Ju-Hee Lee, Ji-Hong Moon, Sung-Wook Kim, You-Jin Lee and Sang-Youel Park

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Oncotarget. 2015; 6:5342-5353. https://doi.org/10.18632/oncotarget.3028

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Abstract

Jin-Young Park1,*, Jae-Kyo Jeong1,2,*, Ju-Hee Lee1,2, Ji-Hong Moon1,2, Sung-Wook Kim1, You-Jin Lee1,2, Sang-Youel Park1,2

1Biosafety Research Institute, College of Veterinary Medicine, Chonbuk National University, Jeonju, Jeonbuk, South Korea

2Department of Bioactive Material Sciences and Research Center of Bioactive Materials, Chonbuk National University, Jeonju, Jeonbuk, South Korea

*These authors have contributed equally to this work

Correspondence to:

Sang-Youel Park, e-mail: sypark@chonbuk.ac.kr

Keywords: PrPc, Hypoxia, TRAIL, HIF-1α, Colon cancer

Received: October 01, 2014     Accepted: January 01, 2015     Published: January 20, 2015

ABSTRACT

Hypoxia decreases cytotoxic responses to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) protein. Cellular prion protein (PrPc) is regulated by HIF-1α in neurons. We hypothesized that PrPc is involved in hypoxia-mediated resistance to TRAIL-induced apoptosis. We found that hypoxia induced PrPc protein and inhibited TRAIL-induced apoptosis. Thus silencing of PrPc increased TRAIL-induced apoptosis under hypoxia. Overexpression of PrPc protein using an adenoviral vector inhibited TRAIL-induced apoptosis. In xenograft model in vivo, shPrPc transfected cells were more sensitive to TRAIL-induced apoptosis than in shMock transfected cells. Molecular chemo-therapy approaches based on the regulation of PrPc expression need to address anti-tumor function of TRAIL under hypoxia. Molecular chemo-therapy approaches based on the regulation of PrPc expression need to address anti-tumor function of TRAIL under hypoxia.


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