Related Experiment Video

Updated: Jan 29, 2026

A Bioluminescent and Fluorescent Orthotopic Syngeneic Murine Model of Androgen-dependent and Castration-resistant Prostate Cancer
07:25

A Bioluminescent and Fluorescent Orthotopic Syngeneic Murine Model of Androgen-dependent and Castration-resistant Prostate Cancer

Published on: March 6, 2018

13.7K

Histone-modifying enzymes as drivers and therapeutic targets in androgen-resistant prostate cancer

Tanaya A Purohit1,2, Kayla Bahr1, Bing Yang1

  • 1Department of Urology, School of Medicine and Public Health, University of Wisconsin, Madison, WI, United States.

Frontiers in Endocrinology
|January 28, 2026
PubMed

Insights

Androgen deprivation therapy resistance in prostate cancer is linked to epigenetic changes. Histone-modifying enzymes (HMEs) drive this progression, suggesting HME inhibitors as a potential therapeutic strategy.

Area of Science:

  • Oncology
  • Epigenetics
  • Molecular Biology

Background:

  • Androgen deprivation therapy (ADT) is a primary treatment for advanced prostate cancer.
  • Most patients eventually develop castration-resistant prostate cancer (CRPC), a difficult-to-treat stage.
  • The mechanisms of ADT resistance are not fully understood, but epigenetic dysregulation is implicated.

Purpose of the Study:

  • To review the role of histone-modifying enzymes (HMEs) and their associated epigenetic modifications in CRPC progression.
  • To discuss the therapeutic potential of HME inhibitors for prostate cancer.

Main Methods:

  • Literature review focusing on epigenetic dysregulation in prostate cancer.
  • Analysis of the contribution of histone PTMs and HMEs to CRPC.
  • Evaluation of HME inhibitors as a therapeutic strategy.

Main Results:

  • Alterations in HMEs and epigenetic dysregulation significantly contribute to prostate cancer progression and resistance to ADT.
  • HMEs regulate chromatin structure and gene expression, impacting androgen resistance.
  • HME inhibitors show therapeutic promise but require context-specific application.

Conclusions:

  • Epigenetic dysregulation by HMEs is a key driver of CRPC.
  • Targeting HMEs offers a novel therapeutic avenue for improving outcomes in advanced prostate cancer.
  • Biomarker-guided strategies and combination therapies are crucial for effective HME inhibitor use.
Keywords:
EZH2 overexpressionNSD2androgen resistancecastration-resistant prostate cancerepigenetics (chromatin remodeling)histone acetylationhistone methylationprostate cancer

More Related Videos

Generation of Prostate Cancer Cell Models of Resistance to the Anti-mitotic Agent Docetaxel06:44

Generation of Prostate Cancer Cell Models of Resistance to the Anti-mitotic Agent Docetaxel

Published on: September 8, 2017

14.0K
Looking for Driver Pathways of Acquired Resistance to Targeted Therapy: Drug Resistant Subclone Generation and Sensitivity Restoring by Gene Knock-down08:59

Looking for Driver Pathways of Acquired Resistance to Targeted Therapy: Drug Resistant Subclone Generation and Sensitivity Restoring by Gene Knock-down

Published on: December 11, 2017

7.6K

Related Concept Videos

Histone Modification02:32

Histone Modification

The histone proteins have a flexible N-terminal tail extending out from the nucleosome. These histone tails are often subjected to post-translational modifications such as acetylation, methylation, phosphorylation, and ubiquitination. Particular combinations of these modifications form “histone codes” that influence the chromatin folding and tissue-specific gene expression.
Acetylation
The enzyme histone acetyltransferase adds acetyl group to the histones. Another enzyme, histone...
16.1K
Histone Modification02:32

Histone Modification

4.5K
Treatment Resistant Cancers02:56

Treatment Resistant Cancers

Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...
3.7K
Histone Variants at the Centromere02:30

Histone Variants at the Centromere

Histone variants are the histone proteins with structural and sequence variations. These variants may be regarded as “mutant” forms that replace their canonical histone counterparts in the nucleosomes. Specific post-translational modifications on the histone variants enable further chromatin complexity and regulate tissue-specific gene expression. The most common histone variants are from histone H2A, H2B, and linker histone H1 families. However, several variants of histone H3...
5.0K
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against...
8.9K
Enzymes02:34

Enzymes

Inside living organisms, enzymes act as catalysts for many biochemical reactions involved in cellular metabolism. The role of enzymes is to reduce the activation energies of biochemical reactions by forming complexes with its substrates. The lowering of activation energies favor an increase in the rates of biochemical reactions.
Enzyme deficiencies can often translate into life-threatening diseases. For example, a genetic abnormality resulting in the deficiency of the enzyme G6PD...
94.6K