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综合生物信息学分析确定ASNS和DDIT3为去势抵抗性前列腺癌的治疗靶点。

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

作者信息

Jung Ae Ryang, Shin Sun, Kim Mee Young, Ha U-Syn, Hong Sung-Hoo, Lee Ji Youl, Kim Sae Woong, Chung Yeun-Jun, Park Yong Hyun

机构信息

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

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

出版信息

Int J Mol Sci. 2024 Feb 29;25(5):2836. doi: 10.3390/ijms25052836.

DOI:10.3390/ijms25052836
PMID:38474084
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10932076/
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 (, , , , , , and ) associated with CRPC progression. Among these hub genes, and were markedly upregulated in CRPC cell lines and CRPC patient samples. The patients with high expression of and showed worse disease-free survival in patients with The Cancer Genome Atlas (TCGA)-prostate adenocarcinoma (PRAD) datasets. Our study revealed a potential association between and 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.

摘要

许多研究已经阐明了去势抵抗性前列腺癌（CRPC）进展的机制及其新的治疗策略。尽管取得了这些进展，但CRPC进展的分子机制仍不清楚，目前尚无有效的CRPC治疗方法。在此，我们对参与CRPC进展的关键基因进行了表征，以深入了解潜在的治疗靶点。我们构建了源自LNCaP的比卡鲁胺耐药前列腺癌细胞，并将其命名为比卡鲁胺R（Bical R）。利用RNA测序来鉴定LNCaP和比卡鲁胺R之间的差异表达基因（DEG）。总共鉴定出631个DEG（302个上调基因和329个下调基因）。使用Cytoscape中的Cytohubba插件来鉴定与CRPC进展相关的7个枢纽基因（、、、、、和）。在这些枢纽基因中，和在CRPC细胞系和CRPC患者样本中显著上调。在癌症基因组图谱（TCGA）-前列腺腺癌（PRAD）数据集中，和高表达的患者无病生存期较差。我们的研究揭示了和与CRPC进展之间的潜在关联。这些结果可能有助于开发潜在的治疗靶点以及CRPC进展的潜在机制，旨在提高CRPC治疗的临床疗效。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c4c/10932076/f7b68aa2a218/ijms-25-02836-g007a.jpg
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