Oncotarget

Research Papers:

Lack of adiponectin and adiponectin receptor 1 contributes to benign prostatic hyperplasia

Shi Fu, Huan Xu, Meng Gu, Chong Liu, Xiang Wan, Yanbo Chen, Qi Chen, Juan Zhou and Zhong Wang _

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Oncotarget. 2017; 8:88537-88551. https://doi.org/10.18632/oncotarget.19877

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Abstract

Shi Fu1,*, Huan Xu1,*, Meng Gu1, Chong Liu1, Xiang Wan1, Yanbo Chen1, Qi Chen1, Juan Zhou1 and Zhong Wang1

1Department of Urology, Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine (SJTUSM), Shanghai 200011, China

*These authors have contributed equally to this work as first author

Correspondence to:

Zhong Wang, email: zhongwang2000@sina.com

Juan Zhou, email: zhoujuan0002@163.com

Keywords: BPH, adiponectin, obesity, AdipoR1, p90RSK

Received: December 20, 2016    Accepted: July 11, 2017    Published: August 03, 2017

ABSTRACT

PURPOSE: The incidence of benign prostatic hyperplasia increases among obese individuals, but few studies have fully explained the underlying mechanisms. Adiponectin has drawn much attention in recent years due to its protective role in obesity-related diseases. Here we aimed to investigate the possible molecular mechanisms and clinical significance of adiponectin in relation to benign prostatic hyperplasia.

METHODS: We analyzed data from 98 Chinese men, including 48 BPH cases and 50 controls in a case-control study. Then, we utilized a tissue microarray analysis to examine expression of AdipoR1 and p-p90RSK in normal and hyperplastic prostate tissues. These studies were followed by various in vitro approaches to examine the anti-proliferation effect and signaling pathways of adiponectin involved in benign prostatic hyperplasia.

RESULTS: Lower serum adiponectin levels were independently associated with larger prostate volume and an increased risk of benign prostatic hyperplasia. Benign prostatic hyperplasia tissues had a decreased expression of AdipoR1 and increased expression of p-p90RSK compared with normal prostate tissues. in vitro, adiponectin inhibited the proliferation of prostatic epithelial and stromal cells and arrested cells in the G0/G1 phase by decreasing phosphorylation of the MEK-ERK-p90RSK axis.

CONCLUSIONS: Our results suggest a possible negative regulatory mechanism in which adiponectin signaling antagonizes ERK-mediated cell proliferation, and a deficiency in adiponectin could facilitate the proliferation of prostate cells and consequently contribute to benign prostatic hyperplasia.


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