Identification of PRDX5 as A Target for The Treatment of Castration‐Resistant Prostate Cancer

Wang, Rong; Mi, Yuanyuan; Ni, Jiang; Wang, Yang; Ding, Lingwen; Ran, Xuebin; Sun, Qiaoyang; Tan, Soo Yong; Koeffler, H Phillip; Feng, Ninghan; Chen, Yong Q

doi:10.1002/advs.202304939

Cited by 2 publications

(1 citation statement)

References 37 publications

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“…A better understanding of these mechanisms provides a good opportunity for discovering therapeutic targets in drug development [ 14 , 15 ]. The identification of potential genes related to CRPC development has been demonstrated [ 16 , 17 ]; however, whether they are sufficiently understood remains to be determined.…”

Section: Introductionmentioning

confidence: 99%

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

Jung,

Shin,

Kim

et al. 2024

IJMS

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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.

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Section: Introductionmentioning

confidence: 99%

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

Jung,

Shin,

Kim

et al. 2024

IJMS

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The Cancer Antioxidant Regulation System in Therapeutic Resistance

Gu,

Mu,

Zheng

et al. 2024

Antioxidants

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Antioxidants play a pivotal role in neutralizing reactive oxygen species (ROS), which are known to induce oxidative stress. In the context of cancer development, cancer cells adeptly maintain elevated levels of both ROS and antioxidants through a process termed “redox reprogramming”. This balance optimizes the proliferative influence of ROS while simultaneously reducing the potential for ROS to cause damage to the cell. In some cases, the adapted antioxidant machinery can hamper the efficacy of treatments for neoplastic diseases, representing a significant facet of the resistance mechanisms observed in cancer therapy. In this review, we outline the contribution of antioxidant systems to therapeutic resistance. We detail the fundamental constituents of these systems, encompassing the central regulatory mechanisms involving transcription factors (of particular importance is the KEAP1/NRF2 signaling axis), the molecular effectors of antioxidants, and the auxiliary systems responsible for NADPH generation. Furthermore, we present recent clinical trials based on targeted antioxidant systems for the treatment of cancer, assessing the potential as well as challenges of this strategy in cancer therapy. Additionally, we summarize the pressing issues in the field, with the aim of illuminating a path toward the emergence of novel anticancer therapeutic approaches by orchestrating redox signaling.

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Identification of PRDX5 as A Target for The Treatment of Castration‐Resistant Prostate Cancer

Cited by 2 publications

References 37 publications

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

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

The Cancer Antioxidant Regulation System in Therapeutic Resistance

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