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长链非编码RNA LOC730101通过抑制miR-1-3p促进前列腺癌对达洛鲁胺的耐药性。

LncRNA LOC730101 Promotes Darolutamide Resistance in Prostate Cancer by Suppressing miR-1-3p.

作者信息

Zhou Tianyi, Nguyen Steven, Wu Jacky, He Bin, Feng Qin

机构信息

Center for Nuclear Receptors and Cell Signaling, Department of Biology and Biochemistry, University of Houston, Houston, TX 77204, USA.

Immunobiology & Transplant Science Center, Houston Methodist Research Institute, Houston, TX 77030, USA.

出版信息

Cancers (Basel). 2024 Jul 20;16(14):2594. doi: 10.3390/cancers16142594.

DOI:10.3390/cancers16142594
PMID:39061232
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11274508/
Abstract

Antiandrogen is part of the standard-of-care treatment option for metastatic prostate cancer. However, prostate cancers frequently relapse, and the underlying resistance mechanism remains incompletely understood. This study seeks to investigate whether long non-coding RNAs (lncRNAs) contribute to the resistance against the latest antiandrogen drug, darolutamide. Our RNA sequencing analysis revealed significant overexpression of LOC730101 in darolutamide-resistant cancer cells compared to the parental cells. Elevated LOC730101 levels were also observed in clinical samples of metastatic castration-resistant prostate cancer (CRPC) compared to primary prostate cancer samples. Silencing LOC730101 with siRNA significantly impaired the growth of darolutamide-resistant cells. Additional RNA sequencing analysis identified a set of genes regulated by LOC730101, including key players in the cell cycle regulatory pathway. We further demonstrated that LOC730101 promotes darolutamide resistance by competitively inhibiting microRNA miR-1-3p. Moreover, by Hi-C sequencing, we found that is located in a topologically associating domain (TAD) that undergoes specific gene induction in darolutamide-resistant cells. Collectively, our study demonstrates the crucial role of the lncRNA LOC730101 in darolutamide resistance and its potential as a target for overcoming antiandrogen resistance in CRPC.

摘要

抗雄激素药物是转移性前列腺癌标准治疗方案的一部分。然而，前列腺癌经常复发，其潜在的耐药机制仍未完全明确。本研究旨在探究长链非编码RNA（lncRNA）是否与对最新抗雄激素药物达洛鲁胺的耐药性有关。我们的RNA测序分析显示，与亲本细胞相比，达洛鲁胺耐药癌细胞中LOC730101显著过表达。与原发性前列腺癌样本相比，在转移性去势抵抗性前列腺癌（CRPC）的临床样本中也观察到LOC730101水平升高。用小干扰RNA（siRNA）沉默LOC730101可显著抑制达洛鲁胺耐药细胞的生长。进一步的RNA测序分析确定了一组受LOC730101调控的基因，包括细胞周期调控途径中的关键因子。我们进一步证明，LOC730101通过竞争性抑制微小RNA miR-1-3p促进达洛鲁胺耐药。此外，通过Hi-C测序，我们发现 位于一个拓扑相关结构域（TAD）中，该结构域在达洛鲁胺耐药细胞中发生特异性基因诱导。总的来说，我们的研究证明了lncRNA LOC730101在达洛鲁胺耐药中的关键作用及其作为克服CRPC抗雄激素耐药靶点的潜力。 （注：原文中“by Hi-C sequencing, we found that is located in...”这里“that”后面缺失内容，我按正常逻辑翻译了，你可根据实际补充完整后再看译文是否符合需求）

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/209b/11274508/1127d717cefe/cancers-16-02594-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/209b/11274508/0f27355bc5f1/cancers-16-02594-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/209b/11274508/78d55eba9f69/cancers-16-02594-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/209b/11274508/0f7d59f7b6f6/cancers-16-02594-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/209b/11274508/0800cb1b8759/cancers-16-02594-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/209b/11274508/28dca97b6c19/cancers-16-02594-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/209b/11274508/1127d717cefe/cancers-16-02594-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/209b/11274508/0f27355bc5f1/cancers-16-02594-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/209b/11274508/78d55eba9f69/cancers-16-02594-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/209b/11274508/0f7d59f7b6f6/cancers-16-02594-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/209b/11274508/0800cb1b8759/cancers-16-02594-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/209b/11274508/28dca97b6c19/cancers-16-02594-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/209b/11274508/1127d717cefe/cancers-16-02594-g006.jpg

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