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

Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

5.5K
Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
5.5K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

3.6K
The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
3.6K
Abnormal Proliferation02:23

Abnormal Proliferation

4.3K
Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
4.3K
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

7.4K
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...
7.4K
Tumor Progression02:07

Tumor Progression

6.1K
Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
6.1K
The Retinoblastoma Gene01:20

The Retinoblastoma Gene

4.0K
Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
The first-ever tumor suppressor gene called Rb was identified in retinoblastoma - a rare eye tumor in children. In inherited forms of the disease, a child inherits one defective copy of the Rb gene, which predisposes them to retinoblastoma. However,...
4.0K

You might also read

Related Articles

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

Sort by
Same author

FTR85 negatively regulates type I IFN antiviral signaling pathway by promoting K48-linked polyubiquitination of IRF3.

Journal of immunology (Baltimore, Md. : 1950)·2026
Same author

HAAO‑derived quinolinic acid fuels FDPS‑dependent AR signaling and sensitizes prostate cancer to combination therapy.

Cell death discovery·2026
Same author

Corylifol A alleviates rheumatoid arthritis by targeting HSP90α and suppressing Wnt/β-catenin signaling.

Biochemical pharmacology·2026
Same author

Common carp Ftr82 positively regulates antiviral innate immunity by promoting Irf3 K63-linked ubiquitination.

Fish & shellfish immunology·2026
Same author

Negative regulation of the NLRP1 inflammasome by B-cell lymphoma-2-like molecule in Cyprinus carpio L.

Fish & shellfish immunology·2026
Same author

CcFTR54 restricts spring viremia of carp virus replication by promoting p62-mediated autophagic degradation of N protein.

Fish & shellfish immunology·2026

Related Experiment Video

Updated: May 10, 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

12.9K

Prostate cancer exploits BRD9-driven metabolic reprogramming to shape the aggressive phenotype.

Ye Lv1, Xinkai Mo2, Ruojia Zhang3

  • 1Shandong Provincial Key Laboratory of Animal Resistance Biology, College of Life Sciences, Shandong Normal University, Jinan, Shandong, China.

Cell Death & Disease
|April 22, 2025
PubMed
Summary

Bromodomain-containing protein 9 (BRD9) helps aggressive prostate cancer (PCa) cells adapt to oxidative stress during castration resistance. Inhibiting BRD9 disrupts this balance, making PCa cells more sensitive to radiotherapy.

More Related Videos

Sequencing Small Non-coding RNA from Formalin-fixed Tissues and Serum-derived Exosomes from Castration-resistant Prostate Cancer Patients
12:13

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

Published on: November 19, 2019

6.7K
Prostate Organoid Cultures as Tools to Translate Genotypes and Mutational Profiles to Pharmacological Responses
08:36

Prostate Organoid Cultures as Tools to Translate Genotypes and Mutational Profiles to Pharmacological Responses

Published on: October 24, 2019

11.0K

Related Experiment Videos

Last Updated: May 10, 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

12.9K
Sequencing Small Non-coding RNA from Formalin-fixed Tissues and Serum-derived Exosomes from Castration-resistant Prostate Cancer Patients
12:13

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

Published on: November 19, 2019

6.7K
Prostate Organoid Cultures as Tools to Translate Genotypes and Mutational Profiles to Pharmacological Responses
08:36

Prostate Organoid Cultures as Tools to Translate Genotypes and Mutational Profiles to Pharmacological Responses

Published on: October 24, 2019

11.0K

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Metabolism

Background:

  • Prostate cancer (PCa) progression to castration-resistant PCa (CRPC) involves adaptation to androgen deprivation (AD) and oxidative stress.
  • The specific oncogenes enabling redox balance maintenance during CRPC remain incompletely understood.

Purpose of the Study:

  • To identify key oncogenes involved in maintaining redox balance during CRPC.
  • To investigate the role of Bromodomain-containing protein 9 (BRD9) in metabolic reprogramming and castration resistance under stress.

Main Methods:

  • Identification of BRD9 as a metabolic checkpoint.
  • Analysis of BRD9's recruitment of nuclear transcription factor-Y A-subunit (NFYA) and induction of glycogen phosphorylase L (PYGL) expression.
  • Assessment of BRD9 inhibition's effect on redox homeostasis and radiosensitivity in PCa cells.

Main Results:

  • BRD9 acts as a metabolic checkpoint, reprogramming cell metabolism to support tumor growth and castration resistance.
  • BRD9, upon oxidation, recruits NFYA to upregulate PYGL, directing glucose to the pentose phosphate pathway for NADPH generation and reactive oxygen species (ROS) clearance.
  • BRD9 inhibition disrupts redox homeostasis, increasing oxidative pressure and sensitizing PCa cells to radiotherapy.

Conclusions:

  • BRD9 is a novel component in antioxidant reprogramming essential for CRPC progression.
  • Targeting BRD9 represents a promising therapeutic strategy for enhancing prostate cancer treatment, particularly in combination with radiotherapy.