Integrated Bioinformatics Analysis Identified ASNS and DDIT3 as the Therapeutic Target in Castrate-Resistant Prostate Cancer

Author:

Jung Ae Ryang1,Shin Sun23,Kim Mee Young1,Ha U-Syn1,Hong Sung-Hoo1,Lee Ji Youl1ORCID,Kim Sae Woong1,Chung Yeun-Jun23ORCID,Park Yong Hyun1ORCID

Affiliation:

1. Department of Urology, Seoul St. Mary’s Hospital, College of Medicine, The Catholic University of Korea, Seoul 06591, Republic of Korea

2. Department of Integrated Research Center for Genome Polymorphism, The Catholic University of Korea, Seoul 06591, Republic of Korea

3. Department of Microbiology, The Catholic University of Korea, Seoul 06591, Republic of Korea

Abstract

Many studies have demonstrated the mechanisms of progression to castration-resistant prostate cancer (CRPC) and novel strategies for its treatment. Despite these advances, the molecular mechanisms underlying the progression to CRPC remain unclear, and currently, no effective treatments for CRPC are available. Here, we characterized the key genes involved in CRPC progression to gain insight into potential therapeutic targets. Bicalutamide-resistant prostate cancer cells derived from LNCaP were generated and named Bical R. RNA sequencing was used to identify differentially expressed genes (DEGs) between LNCaP and Bical R. In total, 631 DEGs (302 upregulated genes and 329 downregulated genes) were identified. The Cytohubba plug-in in Cytoscape was used to identify seven hub genes (ASNS, AGT, ATF3, ATF4, DDIT3, EFNA5, and VEGFA) associated with CRPC progression. Among these hub genes, ASNS and DDIT3 were markedly upregulated in CRPC cell lines and CRPC patient samples. The patients with high expression of ASNS and DDIT3 showed worse disease-free survival in patients with The Cancer Genome Atlas (TCGA)-prostate adenocarcinoma (PRAD) datasets. Our study revealed a potential association between ASNS and DDIT3 and the progression to CRPC. These results may contribute to the development of potential therapeutic targets and mechanisms underlying CRPC progression, aiming to improve clinical efficacy in CRPC treatment.

Funder

National Research Foundation of Korea

Research Fund of Seoul St. Mary’s Hospital, The Catholic University of Korea

Publisher

MDPI AG

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