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
Abnormal Proliferation02:23

Abnormal Proliferation

5.1K
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...
5.1K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

4.6K
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...
4.6K

You might also read

Related Articles

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

Sort by
Same author

Design of Right-Handed D-Sulfonyl-γ-AApeptides with Broad-Spectrum Antimicrobial Activity.

Journal of medicinal chemistry·2026
Same author

Sulfonyl-γ-AAs as Turn Templates Inducing β-Sheet Conformation in Macrocyclic Peptides.

Journal of the American Chemical Society·2026
Same author

α/Sulfonyl-γ-AApeptide foldamers mitigate Alzheimer's disease pathology by stabilizing transient helical domains in Aβ.

Nature communications·2026
Same author

Constructing Metallo-Supramolecular Cuboctahedra Incorporating Flexible Alkyl-Diamines via Postassembly Ligand Exchange.

Inorganic chemistry·2026
Same author

Inhibition of Wnt Signaling Using Axin Peptidomimetics through Direct Targeting of β-Catenin.

Journal of medicinal chemistry·2026
Same author

Structural-Functional Customization of Nanoscale Liposome-in-Liposome Systems: Precision Engineering Methodology and Artificial-Intelligence-Driven Design Prospects.

Research (Washington, D.C.)·2026

Related Experiment Video

Updated: Jan 13, 2026

Testing Targeted Therapies in Cancer using Structural DNA Alteration Analysis and Patient-Derived Xenografts
10:27

Testing Targeted Therapies in Cancer using Structural DNA Alteration Analysis and Patient-Derived Xenografts

Published on: July 25, 2020

7.8K

MDM2 Amplification Enables Selective PROTAC Targeting of Tumor Cells.

Jiandong Chen1, Zainab Fatima1, Lihong Chen1

  • 1Department of Molecular Oncology, Moffitt Cancer Center, Tampa, Florida.

Molecular Cancer Therapeutics
|January 10, 2026
PubMed
Summary

Proteolysis-targeting chimeras (PROTACs) can selectively degrade cancer cells. MDM2 amplification in tumors enhances PROTAC efficacy, suggesting a targeted cancer therapy approach.

More Related Videos

Detection and Monitoring of Tumor Associated Circulating DNA in Patient Biofluids
06:53

Detection and Monitoring of Tumor Associated Circulating DNA in Patient Biofluids

Published on: June 8, 2019

9.1K
Demonstrating a Multi-drug Resistant Mycobacterium tuberculosis Amplification Microarray
07:35

Demonstrating a Multi-drug Resistant Mycobacterium tuberculosis Amplification Microarray

Published on: April 25, 2014

13.2K

Related Experiment Videos

Last Updated: Jan 13, 2026

Testing Targeted Therapies in Cancer using Structural DNA Alteration Analysis and Patient-Derived Xenografts
10:27

Testing Targeted Therapies in Cancer using Structural DNA Alteration Analysis and Patient-Derived Xenografts

Published on: July 25, 2020

7.8K
Detection and Monitoring of Tumor Associated Circulating DNA in Patient Biofluids
06:53

Detection and Monitoring of Tumor Associated Circulating DNA in Patient Biofluids

Published on: June 8, 2019

9.1K
Demonstrating a Multi-drug Resistant Mycobacterium tuberculosis Amplification Microarray
07:35

Demonstrating a Multi-drug Resistant Mycobacterium tuberculosis Amplification Microarray

Published on: April 25, 2014

13.2K

Area of Science:

  • Oncology
  • Molecular Biology
  • Drug Discovery

Background:

  • Proteolysis-targeting chimeras (PROTACs) are novel therapeutics inducing targeted protein degradation.
  • Current PROTACs utilize ubiquitously expressed E3 ligases, limiting tumor specificity.
  • MDM2, involved in the p53 pathway, exhibits tumor-specific amplification in certain cancers.

Purpose of the Study:

  • To investigate MDM2 as a tumor-specific E3 ligase for PROTAC-mediated cancer therapy.
  • To evaluate the efficacy of a benchmark PROTAC (A1874) targeting BRD4 in relation to MDM2 expression.

Main Methods:

  • Analysis of PROTAC compound A1874 activity under varying MDM2 expression conditions.
  • Assessment of PROTAC efficacy in cancer cells with and without MDM2 amplification.
  • Evaluation of cytotoxicity in relation to MDM2 status and p53 pathway activity.

Main Results:

  • PROTAC A1874 activity is dependent on p53-mediated MDM2 induction and inactive in p53-mutant cells.
  • Tumor cells with MDM2 amplification demonstrated ~12-fold higher PROTAC potency.
  • Enhanced cytotoxicity correlated with MDM2 amplification and overexpression.

Conclusions:

  • MDM2 amplification or overexpression in tumors enables selective targeting via PROTACs.
  • This strategy holds promise for increasing therapeutic efficacy and reducing toxicity in cancer treatment.
  • MDM2-targeted PROTACs represent a potential precision medicine approach for specific cancer types.