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PMID: 32931739 Published · ppublish English Journal Article Research Support, N.I.H., Extramural Comment

SETting Up for Epigenetic Regulation of Advanced Prostate Cancer.

Cancer cell ·Vol. 38 ·No. 3 ·2020-00-14 ·Pages 309-311

Thienger P, Rubin MA

Abstract

An outgrowth of therapy-resistant prostate cancers (PCa) with enhanced metastatic potential may be triggered by inhibitors of androgen receptor (AR) signaling, often via epigenetic rewiring. In this issue of Cancer Cell, Yuan et al. demonstrate how SETD2 integrates EZH2 and AMPK signaling pathways to keep PCa metastasis in check.

MeSH Terms
AMP-Activated Protein Kinases Cell Line, Tumor Enhancer of Zeste Homolog 2 Protein/genetics,metabolism Epigenesis, Genetic Gene Expression Regulation, Neoplastic Humans Male Prostatic Neoplasms/genetics Receptors, Androgen/genetics,metabolism
Chemicals
Receptors, Androgen EZH2 protein, human Enhancer of Zeste Homolog 2 Protein AMP-Activated Protein Kinases
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Thienger Phillip
Department for BioMedical Research, University of Bern, Switzerland.
Rubin Mark A
Department for BioMedical Research, University of Bern, Switzerland; Bern Center for Precision Medicine, University of Bern and Inselspital, Bern, Switzerland. Electronic address: mark.rubin@dbmr.unibe.ch.
Conflict of Interest

Declaration of Interests M.A.R. is a co-inventor of U.S. patent 7,229,774, which includes coverage of EZH2 as a prostate cancer biomarker and is currently licensed to Ventana/ROCHE by the University of Michigan.

References (10)
10 references, click to expand
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Article Info
Journal
Cancer cell
Abbr.
Cancer Cell
ISSN
1878-3686
DOI
10.1016/j.ccell.2020.08.009
Email
mark.rubin@dbmr.unibe.ch
Published
2020-00-14
Pages
309-311
Language
English
Region
United States
NLM ID
101130617
PMCID
PMC8404154
Subset
IM
Grants
NCI NIH HHS · P50 CA211024 · United States
Corrections
CommentOn
PMID: 32619406
External Links
PubMed source DOI: 10.1016/j.ccell.2020.08.009 PMC Full Text View journal details
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