Computational drug discovery for castration-resistant prostate cancers through in vitro drug response modeling

Author:

Zhang Weijie12ORCID,Lee Adam M.2ORCID,Jena Sampreeti2,Huang Yingbo2ORCID,Ho Yeung3,Tietz Kiel T.3ORCID,Miller Conor R.3ORCID,Su Mei-Chi2ORCID,Mentzer Joshua2,Ling Alexander L.2,Li Yingming3,Dehm Scott M.3,Huang R. Stephanie12ORCID

Affiliation:

1. Bioinformatics and Computational Biology, University of Minnesota, Minneapolis, MN 55455

2. The Department of Experimental and Clinical Pharmacology, College of Pharmacy, University of Minnesota, Minneapolis, MN 55455

3. Department of Laboratory Medicine and Pathology, The University of Minnesota Medical School, Minneapolis, MN 55455

Abstract

Prostate cancer (PC) is the most frequently diagnosed malignancy and a leading cause of cancer deaths in US men. Many PC cases metastasize and develop resistance to systemic hormonal therapy, a stage known as castration-resistant prostate cancer (CRPC). Therefore, there is an urgent need to develop effective therapeutic strategies for CRPC. Traditional drug discovery pipelines require significant time and capital input, which highlights a need for novel methods to evaluate the repositioning potential of existing drugs. Here, we present a computational framework to predict drug sensitivities of clinical CRPC tumors to various existing compounds and identify treatment options with high potential for clinical impact. We applied this method to a CRPC patient cohort and nominated drugs to combat resistance to hormonal therapies including abiraterone and enzalutamide. The utility of this method was demonstrated by nomination of multiple drugs that are currently undergoing clinical trials for CRPC. Additionally, this method identified the tetracycline derivative COL-3, for which we validated higher efficacy in an isogenic cell line model of enzalutamide-resistant vs. enzalutamide-sensitive CRPC. In enzalutamide-resistant CRPC cells, COL-3 displayed higher activity for inhibiting cell growth and migration, and for inducing G1-phase cell cycle arrest and apoptosis. Collectively, these findings demonstrate the utility of a computational framework for independent validation of drugs being tested in CRPC clinical trials, and for nominating drugs with enhanced biological activity in models of enzalutamide-resistant CRPC. The efficiency of this method relative to traditional drug development approaches indicates a high potential for accelerating drug development for CRPC.

Funder

HHS | NIH | National Cancer Institute

UMN | Clinical and Translational Science Institute, University of Minnesota

UMN | Graduate School, University of Minnesota

University of Minnesota

Publisher

Proceedings of the National Academy of Sciences

Subject

Multidisciplinary

Reference70 articles.

1. R. L. Siegel K. D. Miller H. E. Fuchs A. Jemal Cancer statistics 2022. CA 72 7–33 (2022) 10.3322/caac.21708.

2. M. Kirby C. Hirst E. D. Crawford Characterising the castration-resistant prostate cancer population: A systematic review. Int. J. Clin. Pract. 65 1180–1192 (2011) 10.1111/j.1742-1241.2011.02799.x.

3. L. Puca Patient derived organoids to model rare prostate cancer phenotypes. Nat Commun. 9 2404 (2018) 10.1038/s41467-018-04495-z.

4. W. Abida Genomic correlates of clinical outcome in advanced prostate cancer. Proc. Natl. Acad. Sci. U.S.A. 116 11428–11436 (2019) 10.1073/pnas.1902651116.

5. D. Robinson Integrative clinical genomics of advanced prostate cancer. Cell 161 1215–1228 (2015) 10.1016/j.cell.2015.05.001.

Cited by 3 articles. 订阅此论文施引文献 订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献

同舟云学术

1.学者识别学者识别

2.学术分析学术分析

3.人才评估人才评估

"同舟云学术"是以全球学者为主线,采集、加工和组织学术论文而形成的新型学术文献查询和分析系统,可以对全球学者进行文献检索和人才价值评估。用户可以通过关注某些学科领域的顶尖人物而持续追踪该领域的学科进展和研究前沿。经过近期的数据扩容,当前同舟云学术共收录了国内外主流学术期刊6万余种,收集的期刊论文及会议论文总量共计约1.5亿篇,并以每天添加12000余篇中外论文的速度递增。我们也可以为用户提供个性化、定制化的学者数据。欢迎来电咨询!咨询电话:010-8811{复制后删除}0370

www.globalauthorid.com

TOP

Copyright © 2019-2024 北京同舟云网络信息技术有限公司
京公网安备11010802033243号  京ICP备18003416号-3