Research Papers:

Mitochondrion-associated protein peroxiredoxin 3 promotes benign prostatic hyperplasia through autophagy suppression and pyroptosis activation

Min-Yao Jiang, Zhao-Dong Han, Wenjiao Li, Fei Yue, Jianheng Ye, Bowei Li, Zhiduan Cai, Jian-Ming Lu, Weimin Dong, Xianhan Jiang, Weide Zhong, Huichan He and Leyuan Liu _

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Oncotarget. 2017; 8:80295-80302. https://doi.org/10.18632/oncotarget.17927

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Min-Yao Jiang1,2,*, Zhao-Dong Han1,*, Wenjiao Li2, Fei Yue2, Jianheng Ye1, Bowei Li1, Zhiduan Cai1, Jian-Ming Lu1, Weimin Dong1, Xianhan Jiang3, Weide Zhong1, Huichan He1 and Leyuan Liu2,3,4

1Department of Urology, Guangdong Key Laboratory of Clinical Molecular Medicine and Diagnostics, Guangzhou First People’s Hospital, Guangzhou Medical University, Guangzhou, China

2Institute of Biosciences and Technology, Texas A&M University, Houston, Texas, USA

3Department of Urology, The Fifth Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong Province, China

4Department of Molecular and Cellular Medicine, College of Medicine, Texas A&M University, College Station, Texas, USA

*These authors contributed equally to this work.

Correspondence to:

Leyuan Liu, email: [email protected]

Hui-Chan He, email: [email protected]

Keywords: autophagy, benign prostatic hyperplasia, BPH, caspase 1, LC3

Received: March 12, 2017     Accepted: May 03, 2017     Published: May 17, 2017


Benign prostatic hyperplasia (BPH) is one of the most common diseases in the senior men and age plays an important role in the initiation and development of BPH. Mammalian cells primarily use the autophagy-lysosome system to degrade misfolded/aggregated proteins and dysfunctional organelles such as mitochondria and suppress pyroptosis, a type of cell death that stimulates inflammatory responses and growth of other cells around. Peroxiredoxin 3 (PRDX3) is the only mitochondrion-associated member of peroxiredoxin family enzymes that exert their protective antioxidant role in cells through their peroxidase activity. We hypothesized that PRDX3 may inhibit autophagy to activate pyroptosis to induce growth of prostatic epithelial cells. Here we show that PRDX3 maintained the integrity of mitochondria and its depletion led to an enhancement of oxidative stresses. PRDX3-associated and PRDX3-free mitochondria co-existed in the same cells. PRDX3 expressed at higher levels in prostatic epithelial cells in prostate tissues from BPH patients and BPH-representative cell line than in prostate tissues from healthy donors and a cell line representing normal epithelial cells. PRDX3 suppressed autophagy flux and activated pyroptosis to induce inflammatory responses and stimulate the over-growth of prostate tissues. Therefore, higher levels of PDRX3 in prostatic epithelial cells may promote the initiation and development of BPH through autophagy inhibition and pyroptosis activation.

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