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Suppression of cathepsin a inhibits growth, migration, and invasion by inhibiting the p38 MAPK signaling pathway in prostate cancer

Title
Suppression of cathepsin a inhibits growth, migration, and invasion by inhibiting the p38 MAPK signaling pathway in prostate cancer
Authors
Park, SongKwon, WookbongPark, Jin-KyuBaek, Su-MinLee, Seoung-WooCho, Gil-JaeHa, Yun-SokLee, Jun NyungKwon, Tae GyunKim, Myoung OkRyoo, Zae YoungHan, Se-HyeonHan, Jee EunChoi, Seong-Kyoon
DGIST Authors
Choi, Seong-Kyoon
Issue Date
2020-07
Citation
Archives of Biochemistry and Biophysics, 688, 108407
Type
Article
Article Type
Article
Author Keywords
Cathepsin AProstate cancerCell cycleMetastasisp38 MAPK
Keywords
EPITHELIAL-MESENCHYMAL TRANSITIONEXPRESSIONPROLIFERATIONMETASTASISPROGRESSIONACTIVATIONPROTEASESKINASES
ISSN
0003-9861
Abstract
Prostate cancer has the highest incidence among men in advanced countries, as well as a high mortality rate. Despite the efforts of numerous researchers to identify a gene-based therapeutic target as an effective treatment of prostate cancer, there is still a need for further research. The cathepsin gene family is known to have a close correlation with various cancer types and is highly expressed across these cancer types. This study aimed at investigating the correlation between the cathepsin A (CTSA) gene and prostate cancer. Our findings indicated a significantly elevated level of CTSA gene expression in the tissues of patients with prostate cancer when compared with normal prostate tissues. Furthermore, the knockdown of the CTSA gene in the representative prostate cancer cell lines PC3 and DU145 led to reduced proliferation and a marked reduction in anchorage-independent colony formation, which was shown to be caused by cell cycle arrest in the S phase. In addition, CTSA gene-knockdown prostate cancer cell lines showed a substantial decrease in migration and invasion, as well as a decrease in the marker genes that promote epithelial mesenchymal transition (EMT). Such phenotypic changes in prostate cancer cell lines through CTSA gene suppression were found to be mainly caused by reduced p38 MAPK protein phosphorylation; i.e. the inactivation of the p38 MAPK cell signaling pathway. Tumorigenesis was also found to be inhibited in CTSA gene-knockdown prostate cancer cell lines when a xenograft assay was carried out using Balb/c nude mice, and the p38 MAPK phosphorylation was inhibited in tumor tissues. Thus, the CTSA gene is presumed to play a key role in human prostate cancer tissues through high-level expression, and the suppression of the CTSA gene leads to the inhibition of prostate cancer cell proliferation, colony formation, and metastasis. The mechanism, by which these effects occur, was demonstrated to be the inactivation of the p38 MAPK signaling pathway. © 2020 Elsevier Inc.
URI
http://hdl.handle.net/20.500.11750/11873
DOI
10.1016/j.abb.2020.108407
Publisher
Academic Press
Related Researcher
Files:
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Collection:
Division of Biotechnology1. Journal Articles


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