Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Chromatin Modification in iPS Cells01:32

Chromatin Modification in iPS Cells

Chromatin modification alters gene expression; therefore, scientists can add histone-modifying enzymes, histone variants, and chromatin remodeling complexes to somatic cells to aid reprogramming into pluripotent stem (iPS) cells.
Compact chromatin makes reprogramming difficult. Enzymes, such as histone demethylases and acetyltransferases, are often added during reprogramming to loosen the chromatin, making the DNA more accessible to transcription factors. Molecules that inhibit histone...
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 variants are also...
Cancer Stem Cells and Tumor Maintenance02:40

Cancer Stem Cells and Tumor Maintenance

Early diagnosis and treatment can often cure cancer. However, even with treatment, residual cells called cancer stem cells (CSC) might remain, often causing tumor recurrence. These cancer stem cells possess the potential for self-renewal and multi-lineage differentiation and are often responsible for the therapeutic resistance displayed in most cancers.
Cancer stem cells are thought to originate from tissue-specific normal stem cells or progenitor cells. The normal stem cells usually reside in...
Cancer Stem Cells and Tumor Maintenance02:40

Cancer Stem Cells and Tumor Maintenance

Early diagnosis and treatment can often cure cancer. However, even with treatment, residual cells called cancer stem cells (CSC) might remain, often causing tumor recurrence. These cancer stem cells possess the potential for self-renewal and multi-lineage differentiation and are often responsible for the therapeutic resistance displayed in most cancers.
Cancer stem cells are thought to originate from tissue-specific normal stem cells or progenitor cells. The normal stem cells usually reside in...
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 deacetylase,...
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 deacetylase,...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Effects of the HDAC6/8 Inhibitor MC1568, Alone and in Combination With Fluconazole, in Non-Albicans Candida Species Infections.

MicrobiologyOpen·2026
Same author

Probing Chiral Recognition on Amylose Tris(3,5-Dimethylphenylcarbamate) Using Cinnamyl 2-Aminoanilides: The Subtle Impact of Aliphatic Substituents.

Electrophoresis·2026
Same author

Chronic intranasal URB597 treatment reverts short-term memory deficits in a rat model of metabolic syndrome.

Life sciences·2026
Same author

Development of High-Affinity CHD1 Chromodomain Inhibitors.

Journal of medicinal chemistry·2026
Same author

Development of Biphenyl-Substituted Uracil-Based Hydroxamic Acids (UBHAs) as Potent HDAC Inhibitors with Pro-Apoptotic Activity in Leukemia and Prostate Cancer Cells.

Journal of medicinal chemistry·2026
Same author

Combined computational and classical medicinal chemistry procedure to disclose novel pyrrole-based compounds as potential antituberculosis agents.

Journal of computer-aided molecular design·2026

Related Experiment Video

Updated: May 9, 2026

Isolation of Stem-like Cells from 3-Dimensional Spheroid Cultures
09:06

Isolation of Stem-like Cells from 3-Dimensional Spheroid Cultures

Published on: December 13, 2019

Histone modifications, stem cells and prostate cancer.

Francesco Crea, Pier-Luc Clermont, Antonello Mai

  • 1Experimental Therapeutics, British Columbia Cancer Research Centre, 675 West 10th Avenue, Vancouver, BC, Canada, V5Z 1L3. chelgaso@bccrc.ca.

Current Pharmaceutical Design
|July 30, 2013
PubMed
Summary

Histone modifiers (HMs) like Polycomb group genes (PcGs) are key to prostate cancer (PCa) stem cell self-renewal and treatment resistance. Targeting these epigenetic regulators offers a promising new avenue for PCa therapies.

More Related Videos

Isolation of Cancer Stem Cells From Human Prostate Cancer Samples
07:16

Isolation of Cancer Stem Cells From Human Prostate Cancer Samples

Published on: March 14, 2014

Formation of Human Prostate Epithelium Using Tissue Recombination of Rodent Urogenital Sinus Mesenchyme and Human Stem Cells
08:44

Formation of Human Prostate Epithelium Using Tissue Recombination of Rodent Urogenital Sinus Mesenchyme and Human Stem Cells

Published on: June 22, 2013

Related Experiment Videos

Last Updated: May 9, 2026

Isolation of Stem-like Cells from 3-Dimensional Spheroid Cultures
09:06

Isolation of Stem-like Cells from 3-Dimensional Spheroid Cultures

Published on: December 13, 2019

Isolation of Cancer Stem Cells From Human Prostate Cancer Samples
07:16

Isolation of Cancer Stem Cells From Human Prostate Cancer Samples

Published on: March 14, 2014

Formation of Human Prostate Epithelium Using Tissue Recombination of Rodent Urogenital Sinus Mesenchyme and Human Stem Cells
08:44

Formation of Human Prostate Epithelium Using Tissue Recombination of Rodent Urogenital Sinus Mesenchyme and Human Stem Cells

Published on: June 22, 2013

Area of Science:

  • Epigenetics and Cancer Biology
  • Molecular Oncology
  • Stem Cell Research

Background:

  • Prostate cancer (PCa) often becomes resistant to conventional therapies like chemotherapy and radiation.
  • Prostate tumor-initiating cells (TICs) and cancer repopulating cells (CRCs) are stem-like cells driving PCa initiation, progression, and resistance.
  • Histone modifiers (HMs) regulate gene expression and are crucial for normal and cancer cell function, including stem cell self-renewal.

Purpose of the Study:

  • To explore the critical role of histone modifiers (HMs) in prostate cancer stem cell biology.
  • To investigate the potential of targeting HMs, specifically Polycomb group genes (PcGs) and histone lysine demethylases (KDMs), for novel prostate cancer treatments.

Main Methods:

  • Review of current literature on histone modifiers, Polycomb group genes (PcGs), and histone lysine demethylases (KDMs) in prostate cancer.
  • Analysis of the mechanisms by which PcGs (e.g., PRC1, PRC2) and KDMs regulate gene silencing, stem cell self-renewal, and treatment resistance in prostate cancer.
  • Examination of the therapeutic potential of small molecule inhibitors targeting HMs in prostate cancer models.

Main Results:

  • Polycomb group genes (PcGs), particularly BMI1 (a catalytic component of PRC1), are critical for prostate cancer repopulating cell (CRC) self-renewal and chemotherapy resistance, correlating with poorer prognosis.
  • Pharmacological inhibition of PRC2 has demonstrated a reduction in the tumorigenicity and metastatic potential of prostate CRCs.
  • Certain histone lysine demethylases (KDMs) are emerging as key regulators of TIC/CRC biology, with some small molecule inhibitors showing antitumor activity in PCa cells.

Conclusions:

  • Epigenetic regulation by histone modifiers is fundamental to prostate cancer stem cell biology.
  • Targeting HMs, including PcGs and KDMs, represents a promising therapeutic strategy for overcoming treatment resistance and improving outcomes in prostate cancer.
  • Further investigation into HM inhibitors may lead to novel and effective treatments for advanced prostate cancer.