HDAC inhibitors with potential to overcome drug resistance in castration-resistant prostate cancer

Related Experiment Video

Updated: Sep 22, 2025

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

13.3K

Bernhard Biersack1, Bianca Nitzsche2, Michael Höpfner2

  • 1Organic Chemistry Laboratory, University of Bayreuth, Bayreuth 95440, Germany.

Cancer Drug Resistance (Alhambra, Calif.)
|May 18, 2022
PubMed

Insights

Histone deacetylase (HDAC) inhibitors show promise for castration-resistant prostate cancer (CRPC) but face challenges. This review discusses overcoming drug resistance and developing new HDAC inhibitors for improved CRPC treatment.

Area of Science:

  • Oncology
  • Epigenetics
  • Pharmacology

Background:

  • Epigenetic mechanisms are crucial in cancer development and persistence.
  • Histone deacetylase (HDAC) inhibitors are epigenetic drugs with potential in cancer therapy.
  • Castration-resistant prostate cancer (CRPC) requires novel and effective treatments.

Purpose of the Study:

  • To review current histone deacetylase (HDAC) inhibitors for castration-resistant prostate cancer (CRPC).
  • To discuss strategies for overcoming drug resistance associated with existing HDAC inhibitors.
  • To explore the development of novel HDAC inhibitors and combination therapies for CRPC.

Main Methods:

  • Literature review of epigenetic mechanisms in cancer.
  • Analysis of existing HDAC inhibitors and their efficacy in CRPC.
  • Discussion of drug resistance pathways and potential overcoming strategies.
  • Exploration of novel HDAC inhibitor design and synergistic combination therapies.

Main Results:

  • Approved HDAC inhibitors show promise but have significant drawbacks and limitations.
  • Drug resistance is a major hurdle in HDAC inhibitor therapy for CRPC.
  • Combination treatments with other anticancer drugs may yield synergistic effects.

Conclusions:

  • Developing new HDAC inhibitors is essential to overcome limitations of current drugs.
  • Strategies to overcome drug resistance are critical for effective CRPC treatment.
  • Combination therapies offer a promising avenue for enhanced CRPC treatment outcomes.
Keywords:
HDAC inhibitorsHistone deacetylasescastration-resistant prostate cancerdrug resistance

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

13.5K
Sequencing Small Non-coding RNA from Formalin-fixed Tissues and Serum-derived Exosomes from Castration-resistant Prostate Cancer Patients12:13

Sequencing Small Non-coding RNA from Formalin-fixed Tissues and Serum-derived Exosomes from Castration-resistant Prostate Cancer Patients

Published on: November 19, 2019

6.9K

Related Concept Videos

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
529
Treatment for Pulmonary Arterial Hypertension: Receptor Tyrosine Kinase Inhibitors and Calcium Channel Blockers01:26

Treatment for Pulmonary Arterial Hypertension: Receptor Tyrosine Kinase Inhibitors and Calcium Channel Blockers

Receptor tyrosine kinase inhibitors (TKIs) and calcium channel blockers (CCBs) are two critical categories of drugs employed in the treatment of pulmonary artery hypertension (PAH). PAH is a disease that causes high blood pressure in the pulmonary arteries, resulting in chest pain, fatigue, and shortness of breath.
TKIs, such as imatinib (Gleevec), are particularly effective in tackling the growth and mitogenic factors that become upregulated in PAH patients. These factors contribute to the...
265
Antihypertensive Drugs: Direct Renin Inhibitors01:25

Antihypertensive Drugs: Direct Renin Inhibitors

The renin-angiotensin-aldosterone system (RAAS) is an intricate physiological pathway involving numerous enzymes and hormones, including renin, angiotensin-converting enzyme (ACE), angiotensin I and II, and aldosterone. Imbalances within this system increase the production of angiotensin II and aldosterone. Increased angiotensin II levels promote vasoconstriction and blood pressure elevation. Concurrently, higher aldosterone levels stimulate sodium and water reabsorption in the kidneys,...
853
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...
3.4K
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
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...
7.8K