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去势抵抗性前列腺癌中雄激素受体剪接变体的相对mRNA和蛋白质丰度数据。

Data of relative mRNA and protein abundances of androgen receptor splice variants in castration-resistant prostate cancer.

作者信息

Ma Tianfang, Ungerleider Nathan, Zhang Derek Y, Corey Eva, Flemington Erik K, Dong Yan

机构信息

Department of Structural and Cellular Biology, Tulane University School of Medicine, Tulane Cancer Center, New Orleans, LA, USA.

Department of Pathology, Tulane University School of Medicine, Tulane Cancer Center, New Orleans, LA, USA.

出版信息

Data Brief. 2021 Jan 18;34:106774. doi: 10.1016/j.dib.2021.106774. eCollection 2021 Feb.

DOI:10.1016/j.dib.2021.106774
PMID:33537376
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7843390/
Abstract

These data include secondary analysis of publicly available RNA-seq data from castration-resistant prostate cancer (CRPC) patients as well as RT-qPCR and Western blotting analyses of patient-derived xenograft models and a CRPC cell line. We applied Spearman correlation analysis to assess the relationship between canonical androgen receptor (AR) splicing and alternative AR splicing. We also assessed the ratio of AR splice variants (AR-Vs) to the full-length AR (AR-FL) at the RNA and protein levels by absolute RT-qPCR and Western blotting, respectively. These data are critical for studying the mechanisms underlying upregulated expression of AR-Vs after AR-directed therapies and the importance of AR-Vs to castration-resistant progression of prostate cancer. Data presented here are related to the research article by Ma et al., "Increased transcription and high translation efficiency lead to accumulation of androgen receptor splice variant after androgen deprivation therapy", Cancer Lett. In Press [1].

摘要

这些数据包括对去势抵抗性前列腺癌(CRPC)患者公开可用的RNA测序数据进行的二次分析,以及对患者来源的异种移植模型和一种CRPC细胞系进行的逆转录定量聚合酶链反应(RT-qPCR)和蛋白质免疫印迹分析。我们应用斯皮尔曼相关性分析来评估经典雄激素受体(AR)剪接与选择性AR剪接之间的关系。我们还分别通过绝对RT-qPCR和蛋白质免疫印迹在RNA和蛋白质水平评估了AR剪接变体(AR-Vs)与全长AR(AR-FL)的比例。这些数据对于研究AR导向治疗后AR-Vs表达上调的潜在机制以及AR-Vs对前列腺癌去势抵抗进展的重要性至关重要。此处呈现的数据与Ma等人发表于《癌症通讯》(Cancer Lett.)的研究文章“Increased transcription and high translation efficiency lead to accumulation of androgen receptor splice variant after androgen deprivation therapy”相关,该文章即将发表[1]。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a83f/7843390/10da4ba1700b/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a83f/7843390/9a2dc346b26f/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a83f/7843390/2b89ed78471d/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a83f/7843390/f41100141c88/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a83f/7843390/10da4ba1700b/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a83f/7843390/9a2dc346b26f/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a83f/7843390/2b89ed78471d/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a83f/7843390/f41100141c88/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a83f/7843390/10da4ba1700b/gr4.jpg

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Increased transcription and high translation efficiency lead to accumulation of androgen receptor splice variant after androgen deprivation therapy.雄激素剥夺治疗后,转录增加和高翻译效率导致雄激素受体剪接变体的积累。
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本文引用的文献

1
Increased transcription and high translation efficiency lead to accumulation of androgen receptor splice variant after androgen deprivation therapy.雄激素剥夺治疗后,转录增加和高翻译效率导致雄激素受体剪接变体的积累。
Cancer Lett. 2021 Apr 28;504:37-48. doi: 10.1016/j.canlet.2020.12.037. Epub 2021 Feb 6.
2
A prospective genome-wide study of prostate cancer metastases reveals association of wnt pathway activation and increased cell cycle proliferation with primary resistance to abiraterone acetate-prednisone.一项针对前列腺癌转移的全基因组前瞻性研究显示,wnt 通路激活和细胞周期增殖增加与醋酸阿比特龙-泼尼松的原发性耐药相关。
Ann Oncol. 2018 Feb 1;29(2):352-360. doi: 10.1093/annonc/mdx689.
3
Divergent clonal evolution of castration-resistant neuroendocrine prostate cancer.
去势抵抗性神经内分泌前列腺癌的不同克隆进化
Nat Med. 2016 Mar;22(3):298-305. doi: 10.1038/nm.4045. Epub 2016 Feb 8.
4
Integrative clinical genomics of advanced prostate cancer.晚期前列腺癌的整合临床基因组学
Cell. 2015 May 21;161(5):1215-1228. doi: 10.1016/j.cell.2015.05.001.
5
Mechanisms of the androgen receptor splicing in prostate cancer cells.雄激素受体剪接在前列腺癌细胞中的机制。
Oncogene. 2014 Jun 12;33(24):3140-50. doi: 10.1038/onc.2013.284. Epub 2013 Jul 15.