Research Papers:

Evidence for context-dependent functions of KDM5B in prostate development and prostate cancer

Bigang Liu, Rahul Kumar, Hseuh-Ping Chao, Rashid Mehmood, Yibing Ji, Amanda Tracz and Dean G. Tang _

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Oncotarget. 2020; 11:4243-4252. https://doi.org/10.18632/oncotarget.27818

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Bigang Liu1,*, Rahul Kumar2,*, Hseuh-Ping Chao1,3, Rashid Mehmood2,4, Yibing Ji1, Amanda Tracz1 and Dean G. Tang1,2

1 Department of Epigenetics and Molecular Carcinogenesis, The University of Texas M.D Anderson Cancer Center, Science Park, Smithville, TX, USA

2 Department of Pharmacology & Therapeutics, Roswell Park Comprehensive Cancer Center, Buffalo, NY, USA

3 Livestrong Cancer Institutes, Dell Medical School, The University of Texas at Austin, Austin, TX, USA

4 Department of Life Sciences, College of Science and General Studies, Alfaisal University, Takhasusi Street, Riyadh, Saudi Arabia

* These authors contributed equally to this work

Correspondence to:

Dean G. Tang,email: [email protected]

Keywords: KDM5B; prostate cancer; prostate development; hyperplasia; epigenetics

Received: August 20, 2020     Accepted: October 29, 2020     Published: November 17, 2020

Copyright: © 2020 Liu et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.


Prostate cancer (PCa) is one of the leading causes of cancer-related deaths worldwide. Prostate tumorigenesis and PCa progression involve numerous genetic as well as epigenetic perturbations. Histone modification represents a fundamental epigenetic mechanism that regulates diverse cellular processes, and H3K4 methylation, one such histone modification associated with active transcription, can be reversed by dedicated histone demethylase KDM5B (JARID1B). Abnormal expression and functions of KDM5B have been implicated in several cancer types including PCa. Consistently, our bioinformatics analysis reveals that the KDM5B mRNA levels are upregulated in PCa compared to benign prostate tissues, and correlate with increased tumor grade and poor patient survival, supporting an oncogenic function of KDM5B in PCa. Surprisingly, however, when we generated prostate-specific conditional Kdm5b knockout mice using probasin (Pb) promoter-driven Cre: loxP system, we observed that Kdm5b deletion did not affect normal prostate development but instead induced mild hyperplasia. These results suggest that KDM5B may possess context-dependent roles in normal prostate development vs. PCa development and progression.

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