Research Paper Volume 13, Issue 3 pp 3202—3217

GV1001 interacts with androgen receptor to inhibit prostate cell proliferation in benign prostatic hyperplasia by regulating expression of molecules related to epithelial-mesenchymal transition

Yejin Kim1,2, *, , Dahae Lee1, *, , Hyejung Jo1, *, , Cheolhyeon Go1, , Jongwon Yang1, , Dongmin Kang3, , Jae Seung Kang1,2, ,

  • 1 Department of Anatomy, Seoul National University College of Medicine, Seoul, Republic of Korea
  • 2 Institute of Allergy and Clinical Immunology, Seoul National University Medical Research Center, Seoul, Republic of Korea
  • 3 Department of Psychological and Brain Sciences, College of Arts and Sciences, Boston University, Boston, MA 02215, USA
* Equal contribution

Received: March 19, 2020       Accepted: October 20, 2020       Published: February 4, 2021
How to Cite

Copyright: © 2021 Kim et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.


Prostate cell proliferation, driven by testosterone, is a major characteristic of benign prostatic hyperplasia (BPH). GV1001, a human telomerase reverse transcriptase catalytic subunit, is an injectable formulation used as a cancer vaccine. It functions as a cell penetrating peptide to regulate cell proliferation. Here, we found that GV1001 effectively suppressed proliferation of prostatic stromal myofibroblasts (WPMY-1) and prostatic epithelial cells (RWPE-1 and WPE-NA22) treated with dihydrotestosterone. Also, GV1001 bound to androgen receptors (ARs) in the cytosol of stromal and epithelial cells. In an experimental animal model implanted with an infusion pump for spontaneous and continuous release of testosterone, revealed that GV1001 reduced prostatic hypertrophy and inhibited the cell proliferation and the expression of Ki67, proliferating cell nuclear antigen, and prostate specific antigen. In addition, GV1001 prevented fibrosis of the prostate by downregulating expression of prostatic epithelial-mesenchymal transition (EMT)-related proteins such as transforming growth factor (TGF)-β, Snail, Slug, N-cadherin, and Vimentin, and by up-regulating E-cadherin. Taken together, these results suggest that GV1001, which suppresses TGF-β-mediated EMT by outcompeting testosterone for binding to AR, is a potential therapeutic drug for BPH accompanied by prostatic fibrosis.


BPH: benign prostatic hyperplasia; TGF: transforming growth factor; TNF: tumor necrosis factor; hTERT: human telomerase catalytic subunit; DHT: dihydrotestosterone; AR: androgen receptor; PCNA: proliferating cell nuclear antigen; PSA: prostate specific antigen; EMT: epithelial-mesenchymal transition.