Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2018;4(2):101-115.
doi: 10.1007/s40610-018-0095-9. Epub 2018 Apr 18.

Epigenetic Regulation in Prostate Cancer Progression

Affiliations
Review

Epigenetic Regulation in Prostate Cancer Progression

Katia Ruggero et al. Curr Mol Biol Rep. 2018.

Abstract

Purpose of review: An important number of newly identified molecular alterations in prostate cancer affect gene encoding master regulators of chromatin biology epigenetic regulation. This review will provide an updated view of the key epigenetic mechanisms underlying prostate cancer progression, therapy resistance, and potential actionable mechanisms and biomarkers.

Recent findings: Key players in chromatin biology and epigenetic master regulators has been recently described to be crucially altered in metastatic CRPC and tumors that progress to AR independency. As such, epigenetic dysregulation represents a driving mechanism in the reprograming of prostate cancer cells as they lose AR-imposed identity.

Summary: Chromatin integrity and accessibility for transcriptional regulation are key features altered in cancer progression, and particularly relevant in nuclear hormone receptor-driven tumors like prostate cancer. Understanding how chromatin remodeling dictates prostate development and how its deregulation contributes to prostate cancer onset and progression may improve risk stratification and treatment selection for prostate cancer patients.

Keywords: Androgen receptor; Chromatin biology; Drug targets; Epigenetics; Prostate cancer; Transcriptional regulation.

PubMed Disclaimer

Conflict of interest statement

Compliance with Ethical StandardsKatia Ruggero, Sonia Farran-Matas, Adrian Martinez-Tebar, and Alvaro Aytes declare no conflicts of interest.This article does not contain any studies with human or animal subjects performed by any of the authors.

References

    1. Li N, Xue W, Yuan H, Dong B, Ding Y, Liu Y, et al. AKT-mediated stabilization of histone methyltransferase WHSC1 promotes prostate cancer metastasis. J Clin Invest. 2017;127(4):1284–1302. doi: 10.1172/JCI91144. - DOI - PMC - PubMed
    1. Ezponda T, Popovic R, Shah MY, Martinez-Garcia E, Zheng Y, Min DJ, et al. The histone methyltransferase MMSET/WHSC1 activates TWIST1 to promote an epithelial-mesenchymal transition and invasive properties of prostate cancer. Oncogene. 2013;32(23):2882–90. - PMC - PubMed
    1. Asangani IA, Ateeq B, Cao Q, Dodson L, Pandhi M, Kunju LP, et al. Characterization of the EZH2-MMSET histone methyltransferase regulatory axis in cancer. Mol Cell. 2013;49(1):80–93. - PMC - PubMed
    1. Yang YA, Yu J. EZH2, an epigenetic driver of prostate cancer. Protein Cell. 2013;4(5):331–341. doi: 10.1007/s13238-013-2093-2. - DOI - PMC - PubMed
    1. Wu C, Jin X, Yang J, Yang Y, He Y, Ding L, et al. Inhibition of EZH2 by chemo- and radiotherapy agents and small molecule inhibitors induces cell death in castration-resistant prostate cancer. Oncotarget. 2016;7(3):3440–52. - PMC - PubMed