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

Induced Pluripotent Stem Cells01:06

Induced Pluripotent Stem Cells

3.9K
Stem cells are undifferentiated cells that divide and produce different cell types. Ordinarily, cells that have differentiated into a specific cell type are terminally differentiated; however, scientists have found a way to reprogram these mature cells so that they dedifferentiate and return to an unspecialized, proliferative state. These cells are pluripotent like embryonic stem cells—able to produce all cell types—and are called induced pluripotent stem cells (iPSCs).
Somatic...
3.9K
Treatment Resistant Cancers02:56

Treatment Resistant Cancers

3.2K
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...
3.2K
Replicative Cell Senescence02:15

Replicative Cell Senescence

3.6K
Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds...
3.6K
Mismatch Repair01:20

Mismatch Repair

4.7K
Organisms are capable of detecting and fixing nucleotide mismatches that occur during DNA replication. This sophisticated process requires identifying the new strand and replacing the erroneous bases with correct nucleotides. Mismatch repair is coordinated by many proteins in both prokaryotes and eukaryotes.
The Mutator Protein Family Plays a Key Role in DNA Mismatch Repair
The human genome has more than 3 billion base pairs of DNA per cell. Prior to cell division, that vast amount of genetic...
4.7K
The DNA Replication Fork01:02

The DNA Replication Fork

35.3K
An organism’s genome needs to be duplicated in an efficient and error-free manner for its growth and survival. The replication fork is a Y-shaped active region where two strands of DNA are separated and replicated continuously. The coupling of DNA unzipping and complementary strand synthesis is a characteristic feature of a replication fork.   Organisms with small circular DNA, such as E. coli, often have a single origin of replication; therefore, they have only two replication...
35.3K
DNA Damage can Stall the Cell Cycle02:37

DNA Damage can Stall the Cell Cycle

9.0K
In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
9.0K

You might also read

Related Articles

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

Sort by
Same author

The effects of high-intensity interval training on executive function in children and adolescents: a systematic review and meta-analysis.

Frontiers in psychology·2026
Same author

EphB4 inhibition defines a druggable synthetic-lethal vulnerability in MYC-driven triple-negative breast cancer.

Cell death & disease·2026
Same author

Oxymatrine: Hepatoprotective Effects of a Multitarget Natural Alkaloid.

Journal of agricultural and food chemistry·2026
Same author

Analysis of cardiac dynamic global function.

JRSM cardiovascular disease·2026
Same author

Associations between 12 triglyceride-glucose (TyG)-related indices and circadian syndrome among middle-aged and elderly Chinese adults ‒ A cross-sectional analysis of the CHARLS cohort.

Nutricion hospitalaria·2026
Same author

Engineered Bacteroides thetaiotaomicron sense gut inflammation and deliver therapeutic molecules to alleviate colitis in mice.

Nature microbiology·2026

Related Experiment Video

Updated: May 17, 2025

A Data Integration Workflow to Identify Drug Combinations Targeting Synthetic Lethal Interactions
07:40

A Data Integration Workflow to Identify Drug Combinations Targeting Synthetic Lethal Interactions

Published on: May 27, 2021

4.1K

Exploiting replication stress for synthetic lethality in MYC-driven cancers.

Yuan Zhang1,2, Meng Ye1,2, Xin Luan1,2

  • 1School of Pharmacy, Guangdong Pharmaceutical University Guangzhou 510006, Guangdong, China.

American Journal of Cancer Research
|May 15, 2025
PubMed
Summary

Targeting MYC-driven cancers involves exploiting their replication stress. Interfering with cancer cell survival mechanisms induces synthetic lethality, offering new therapeutic strategies for MYC-overexpressing malignancies.

Keywords:
DNA replication stressMYCsynthetic lethality

More Related Videos

Pooled shRNA Library Screening to Identify Factors that Modulate a Drug Resistance Phenotype
14:51

Pooled shRNA Library Screening to Identify Factors that Modulate a Drug Resistance Phenotype

Published on: June 17, 2022

3.1K
Quantifying Replication Stress in Ovarian Cancer Cells Using Single-Stranded DNA Immunofluorescence
06:25

Quantifying Replication Stress in Ovarian Cancer Cells Using Single-Stranded DNA Immunofluorescence

Published on: February 10, 2023

2.0K

Related Experiment Videos

Last Updated: May 17, 2025

A Data Integration Workflow to Identify Drug Combinations Targeting Synthetic Lethal Interactions
07:40

A Data Integration Workflow to Identify Drug Combinations Targeting Synthetic Lethal Interactions

Published on: May 27, 2021

4.1K
Pooled shRNA Library Screening to Identify Factors that Modulate a Drug Resistance Phenotype
14:51

Pooled shRNA Library Screening to Identify Factors that Modulate a Drug Resistance Phenotype

Published on: June 17, 2022

3.1K
Quantifying Replication Stress in Ovarian Cancer Cells Using Single-Stranded DNA Immunofluorescence
06:25

Quantifying Replication Stress in Ovarian Cancer Cells Using Single-Stranded DNA Immunofluorescence

Published on: February 10, 2023

2.0K

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Genetics

Background:

  • The oncoprotein MYC is overexpressed in over 70% of human cancers, regulating gene transcription.
  • MYC is a promising cancer therapy target, but lacks approved drugs due to its undefined druggable domain and nuclear localization.
  • MYC-overexpressing cancers face replication stress from increased origin firing, nucleotide depletion, replication-transcription conflicts, and reactive oxygen species (ROS).

Purpose of the Study:

  • To review recent advances in using replication stress for synthetic lethality in MYC-driven cancers.
  • To discuss current strategies targeting replication stress.
  • To highlight new therapeutic opportunities for MYC-driven malignancies.

Main Methods:

  • Review of current scientific literature on MYC, replication stress, and synthetic lethality.
  • Analysis of compensatory mechanisms in MYC-overexpressing cancer cells.
  • Discussion of therapeutic strategies targeting replication stress pathways.

Main Results:

  • MYC-overexpressing cancer cells exhibit significant replication stress.
  • MYC activates compensatory pathways (DNA repair, cell cycle checkpoints, metabolic reprogramming) to manage this stress.
  • Interfering with these compensatory pathways leads to synthetic lethality in MYC-driven cancer cells.

Conclusions:

  • Leveraging replication stress presents a promising synthetic lethality strategy for MYC-driven cancers.
  • Targeting compensatory pathways offers new avenues for developing MYC-targeted therapies.
  • Further research into replication stress mechanisms can guide the development of novel cancer treatments.