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

Targeted Cancer Therapies02:57

Targeted Cancer Therapies

8.6K
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...
8.6K
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

9.4K
Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
9.4K
Treatment Resistant Cancers02:56

Treatment Resistant Cancers

3.7K
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

You might also read

Related Articles

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

Sort by
Same author

High-resolution reconstruction of cell-type-specific transcriptional regulatory processes from bulk sequencing samples.

Nature biotechnology·2026
Same author

Promoter reinforcement supports transcriptional resilience in drug-resistant cancer.

Nature structural & molecular biology·2026
Same author

Retraction Note: NSD2 targeting reverses plasticity and drug resistance in prostate cancer.

Nature·2026
Same author

Optimized Ex Vivo Human Liver Slice Culture Maintains Extended Viability and Function for Hepatotoxicity Testing.

Advanced science (Weinheim, Baden-Wurttemberg, Germany)·2026
Same author

Covalent pan-TEAD inhibitors block YAP activity and demonstrate brain penetrance in a Hippo-dependent cancer model.

Nature communications·2026
Same author

Phosphatidylserine and RhoB connect PI4P and PA metabolism to maintain plasma membrane identity.

The Journal of cell biology·2026

Related Experiment Video

Updated: Jan 17, 2026

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

7.2K

A Double-Negative Prostate Cancer Subtype Is Vulnerable to SWI/SNF-Targeting Degrader Molecules.

Phillip Thienger1, Irene Paassen1, Xiaosai Yao2,3

  • 1Department for Biomedical Research, University of Bern, Bern, Switzerland.

Cancer Research
|January 14, 2026
PubMed
Summary

Proteolysis targeting chimera (PROTAC) therapies targeting SWI/SNF ATPases show promise in treating castration-resistant prostate cancer (CRPC). These therapies are effective against both AR-dependent and WNT signaling-dependent CRPC subtypes.

More Related Videos

Virus Delivery of CRISPR Guides to the Murine Prostate for Gene Alteration
06:21

Virus Delivery of CRISPR Guides to the Murine Prostate for Gene Alteration

Published on: April 27, 2018

9.1K
A New Technique for Treating Low-risk Prostate Cancer—Super Active Surveillance
05:19

A New Technique for Treating Low-risk Prostate Cancer—Super Active Surveillance

Published on: November 7, 2025

676

Related Experiment Videos

Last Updated: Jan 17, 2026

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

7.2K
Virus Delivery of CRISPR Guides to the Murine Prostate for Gene Alteration
06:21

Virus Delivery of CRISPR Guides to the Murine Prostate for Gene Alteration

Published on: April 27, 2018

9.1K
A New Technique for Treating Low-risk Prostate Cancer—Super Active Surveillance
05:19

A New Technique for Treating Low-risk Prostate Cancer—Super Active Surveillance

Published on: November 7, 2025

676

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Therapeutics

Background:

  • Proteolysis targeting chimera (PROTAC) therapies targeting SWI/SNF ATPases interfere with androgen receptor (AR) signaling in AR-dependent castration-resistant prostate cancer (CRPC-AR).
  • The efficacy of SWI/SNF-targeting agents in AR-negative CRPC remains largely unexplored.
  • AR-negative CRPC, particularly the WNT signaling-dependent subtype (CRPC-WNT), represents a significant unmet clinical need.

Purpose of the Study:

  • To investigate the therapeutic potential of SWI/SNF-targeting agents in AR-negative CRPC.
  • To elucidate the mechanisms by which SWI/SNF depletion affects CRPC-WNT cells.
  • To identify novel therapeutic strategies for advanced prostate cancer.

Main Methods:

  • Treatment of CRPC cell lines and organoid models with SWI/SNF-targeting PROTACs.
  • Assessment of cell viability and signaling pathway alterations.
  • Depletion of SWI/SNF ATPase SMARCA4 and analysis of its downstream targets, including TCF7L2 and MAPK signaling.

Main Results:

  • SWI/SNF-targeting PROTAC treatment reduced the viability of both CRPC-AR and CRPC-WNT cells.
  • SMARCA4 depletion in CRPC-WNT cells interfered with the transcriptional regulator TCF7L2.
  • TCF7L2 was found to maintain proliferation in CRPC-WNT via the MAPK signaling axis.

Conclusions:

  • SWI/SNF-targeting therapies are effective against both AR-dependent and WNT-dependent CRPC.
  • Perturbing TCF7L2 DNA binding or inhibiting MAPK signaling presents a viable therapeutic strategy for CRPC-WNT.
  • These findings offer a mechanistic basis for novel treatment approaches in advanced prostate cancer.