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前列腺癌中与雄激素受体相关的非编码RNA

Androgen Receptor-Related Non-coding RNAs in Prostate Cancer.

作者信息

Yang Yongyong, Liu Kilia Y, Liu Qi, Cao Qi

机构信息

Department of Urology, Feinberg School of Medicine, Northwestern University, Chicago, IL, United States.

Robert H. Lurie Comprehensive Cancer Center, Feinberg School of Medicine, Northwestern University, Chicago, IL, United States.

出版信息

Front Cell Dev Biol. 2021 Apr 1;9:660853. doi: 10.3389/fcell.2021.660853. eCollection 2021.

Abstract

Prostate cancer (PCa) is the second leading cause of cancer-related death among men in the United States. Androgen receptor (AR) signaling is the dominant oncogenic pathway in PCa and the main strategy of PCa treatment is to control the AR activity. A large number of patients acquire resistance to Androgen deprivation therapy (ADT) due to AR aberrant activation, resulting in castration-resistant prostate cancer (CRPC). Understanding the molecular mechanisms underlying AR signaling in the PCa is critical to identify new therapeutic targets for PCa patients. The recent advances in high-throughput RNA sequencing (RNA-seq) techniques identified an increasing number of non-coding RNAs (ncRNAs) that play critical roles through various mechanisms in different diseases. Some ncRNAs have shown great potentials as biomarkers and therapeutic targets. Many ncRNAs have been investigated to regulate PCa through direct association with AR. In this review, we aim to comprehensively summarize recent findings of the functional roles and molecular mechanisms of AR-related ncRNAs as AR regulators or targets in the progression of PCa.

摘要

前列腺癌(PCa)是美国男性癌症相关死亡的第二大主要原因。雄激素受体(AR)信号传导是PCa中的主要致癌途径,PCa治疗的主要策略是控制AR活性。由于AR异常激活,大量患者对雄激素剥夺疗法(ADT)产生耐药性,导致去势抵抗性前列腺癌(CRPC)。了解PCa中AR信号传导的分子机制对于确定PCa患者的新治疗靶点至关重要。高通量RNA测序(RNA-seq)技术的最新进展发现了越来越多的非编码RNA(ncRNA),它们通过各种机制在不同疾病中发挥关键作用。一些ncRNA作为生物标志物和治疗靶点显示出巨大潜力。许多ncRNA已被研究通过与AR直接关联来调节PCa。在本综述中,我们旨在全面总结AR相关ncRNA作为PCa进展中的AR调节剂或靶点的功能作用和分子机制的最新发现。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ffc/8049439/f5f4040a9487/fcell-09-660853-g001.jpg

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