JNK promotes the progression of castration-resistant prostate cancer

  • Yigeng Feng Surgical Department I (Urology Department), LONGHUA Hospital Shanghai University of Traditional Chinese Medicine, Xuhui District, Shanghai 200032, China
  • Hongwen Cao Surgical Department I (Urology Department), LONGHUA Hospital Shanghai University of Traditional Chinese Medicine, Xuhui District, Shanghai 200032, China
  • Dan Wang Surgical Department I (Urology Department), LONGHUA Hospital Shanghai University of Traditional Chinese Medicine, Xuhui District, Shanghai 200032, China
  • Lei Chen Surgical Department I (Urology Department), LONGHUA Hospital Shanghai University of Traditional Chinese Medicine, Xuhui District, Shanghai 200032, China https://orcid.org/0000-0002-6701-2300
  • Renjie Gao Surgical Department I (Urology Department), LONGHUA Hospital Shanghai University of Traditional Chinese Medicine, Xuhui District, Shanghai 200032, China
  • Peng Sun Surgical Department I (Urology Department), LONGHUA Hospital Shanghai University of Traditional Chinese Medicine, Xuhui District, Shanghai 200032, China
DOI: https://doi.org/10.18388/abp.2020_6610

Abstract

Background: Prostate cancer is one of the most common cancers in men worldwide. This study aims to elucidate the roles of c-Jun N-terminal kinase (JNK) in the progression of castration-resistant prostate cancer (CRPC). Methods: JNK overexpressing and knockdown cell lines were established on the PC-3 prostate cell line. qPCR and Western blotting were performed to determine the mRNA and protein levels of target genes in prostate tissues and cell lines. MTT and Matrigel invasion assays were conducted to evaluate the cell viability and invasive ability, respectively. The Kaplan-Meier estimator was performed to estimate the overall survival rate and second progression-free survival rate. Pearson’s correlation coefficient was used to evaluate the relationship between JNK and prostate-specific antigen (PSA). Results: Relative JNK expression was correlated with Gleason score and PSA value in patients with CRPC. Kaplan-Meier analysis revealed that patients with low JNK expression exhibited high overall survival and second progression-free survival rate. In vitro assays demonstrated that JNK overexpression promoted cell viability and invasion as well as the protein expressions of extracellular signal-regulated kinase (ERK) and matrix metalloproteinase 1 (MMP1) in PC-3 cell lines. Conclusions: JNK overexpression promotes the development of CRPC via the regulation of ERK and MMP1.

Published
2023-12-15
Issue
Vol. 70 No. 4 (2023)
Section
Articles

Copyright (c) 2023 Yigeng Feng, Hongwen Cao, Dan Wang, Lei Chen, Renjie Gao, Peng Sun

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