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

Anaphase Promoting Complex00:50

Anaphase Promoting Complex

3.5K
The stepwise destruction of specific proteins is necessary for the progression and completion of the cell cycle. Such proteins are ubiquitinated by ubiquitin ligases and then subsequently destroyed by the proteasome. The SCF (Skp1/Cullin/F-box) and the anaphase-promoting complex (APC) are two important ubiquitin ligases involved in cell cycle progression. While SCF is active throughout the cell cycle, APC gets activated during metaphase to anaphase transition. Cdc20 or Cdh1 binds to APC and...
3.5K
Abnormal Proliferation02:23

Abnormal Proliferation

5.3K
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...
5.3K
Separation of Sister Chromatids02:17

Separation of Sister Chromatids

4.6K
At the transition from prophase to metaphase, there is a reduction in cohesion along the chromosomal arms, resulting in the resolution of sister chromatids. However, residual cohesin connections remain to hold the sister chromatids together until the transition from metaphase to anaphase. The residual connection prevents any premature separation of sister chromatids, blocking the risks of aneuploidy within the daughter cells.
At the onset of anaphase, separase, a proteolytic enzyme, is...
4.6K
DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

10.3K
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...
10.3K
DNA Damage Can Stall the Cell Cycle02:36

DNA Damage Can Stall the Cell Cycle

3.3K
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...
3.3K
Cancers Originate from Somatic Mutations in a Single Cell02:21

Cancers Originate from Somatic Mutations in a Single Cell

15.2K
Cancer arises from mutations in the critical genes that allow healthy cells to escape cell cycle regulation and acquire the ability to proliferate indefinitely. Though originating from a single mutation event in one of the originator cells, cancer progresses when the mutant cell lines continue to gain more and more mutations, and finally, become malignant. For example, chronic myelogenous leukemia (CML) develops initially as a non-lethal increase in white blood cells, which progressively...
15.2K

You might also read

Related Articles

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

Sort by
Same author

Feasibility of <i>PIK3CA</i> Mutation Detection via Microfluidic Isolation of Disseminated Tumor Cells from Bone Marrow in Breast Cancer Patients.

Geburtshilfe und Frauenheilkunde·2026
Same author

NMR-based serum metabolite and lipoprotein profiling for endometriosis across clinically relevant and physiological comparator settings: assessment of diagnostic utility and exploratory biological signals.

BMC medicine·2026
Same author

Long-Term Outcomes From a Decade of Donation After Circulatory Death Heart Transplantation in Australia.

JACC. Heart failure·2026
Same author

Endometrial organoid and stromal cultures demonstrate donor-derived cellular origin of the endometrium after uterus transplantation.

Frontiers in cell and developmental biology·2026
Same author

Subclonal immune evasion in non-small cell lung cancer.

Cancer cell·2026
Same author

Tissue-specific fibroblast lipid cues impose the rate of epithelial cancer invasion.

Nature metabolism·2026
Same journal

DNA, Peptide Vaccines Advance Against GBM.

Cancer discovery·2026
Same journal

AKR1C1 Promotes ADC Resistance by Altering Uptake and Export.

Cancer discovery·2026
Same journal

Acquisition of Centromeric Features Supports Telomere Integrity.

Cancer discovery·2026
Same journal

Germline CDK12 variants in aggressive prostate cancer.

Cancer discovery·2026
Same journal

Type II JAK2 Inhibitor Gets Off to a Strong Start.

Cancer discovery·2026
Same journal

Pancreatic Cancer: Translating Tumor Biology into Actionability.

Cancer discovery·2026
See all related articles

Related Experiment Video

Updated: Mar 9, 2026

Generation and Isolation of Cell Cycle-arrested Cells with Complex Karyotypes
05:22

Generation and Isolation of Cell Cycle-arrested Cells with Complex Karyotypes

Published on: April 13, 2018

11.1K

APC/C Dysfunction Limits Excessive Cancer Chromosomal Instability.

Laurent Sansregret1, James O Patterson1, Sally Dewhurst1

  • 1The Francis Crick Institute, London, United Kingdom.

Cancer Discovery
|January 11, 2017
PubMed
Summary
This summary is machine-generated.

Cancer cells balance chromosomal instability (CIN) with mitosis duration. Partial anaphase-promoting complex/cyclosome (APC/C) dysfunction suppresses errors, aiding adaptation and resistance to cancer therapies.

More Related Videos

Long-term Live-cell Imaging to Assess Cell Fate in Response to Paclitaxel
08:29

Long-term Live-cell Imaging to Assess Cell Fate in Response to Paclitaxel

Published on: May 14, 2018

10.6K
Capturing Common Fragile Site Breaks by Native &#947;H2A.X ChIP
09:46

Capturing Common Fragile Site Breaks by Native γH2A.X ChIP

Published on: January 24, 2025

761

Related Experiment Videos

Last Updated: Mar 9, 2026

Generation and Isolation of Cell Cycle-arrested Cells with Complex Karyotypes
05:22

Generation and Isolation of Cell Cycle-arrested Cells with Complex Karyotypes

Published on: April 13, 2018

11.1K
Long-term Live-cell Imaging to Assess Cell Fate in Response to Paclitaxel
08:29

Long-term Live-cell Imaging to Assess Cell Fate in Response to Paclitaxel

Published on: May 14, 2018

10.6K
Capturing Common Fragile Site Breaks by Native &#947;H2A.X ChIP
09:46

Capturing Common Fragile Site Breaks by Native γH2A.X ChIP

Published on: January 24, 2025

761

Area of Science:

  • Cell Biology
  • Genetics
  • Cancer Research

Background:

  • Intercellular heterogeneity and chromosomal instability (CIN) drive tumor heterogeneity and drug resistance.
  • Paradoxically, extreme CIN can correlate with improved cancer outcomes, suggesting a balance between adaptation and genomic instability.
  • Understanding CIN-survival factors is crucial for cancer treatment strategies.

Purpose of the Study:

  • To identify factors that promote cancer cell survival despite chromosomal instability (CIN).
  • To investigate the role of the anaphase-promoting complex/cyclosome (APC/C) in regulating mitosis and CIN.
  • To explore the implications of APC/C modulation for cancer drug resistance.

Main Methods:

  • Functional genomics screening in diploid cells.
  • Genome editing, including CRISPR-mediated gene modification.
  • Pharmacologic approaches to induce and assess chromosome segregation errors.
  • Analysis of APC/C subunit mutations (e.g., CDC27) and their impact on CIN.

Main Results:

  • Partial APC/C dysfunction was found to lengthen mitosis and suppress chromosome segregation errors.
  • APC/C impairment conferred resistance to MPS1 inhibitors, suggesting a mechanism for therapy resistance.
  • Specific cancer somatic mutations in CDC27 reduced segregation errors, while reversing a nonsense mutation increased CIN.
  • Mitotic duration, modulated by APC/C activity, dynamically influences CIN and cancer cell fitness.

Conclusions:

  • Cancers balance the evolutionary benefits of CIN against the fitness costs of genomic instability.
  • Modulating mitotic duration via APC/C activity is a key mechanism for cancer cells to optimize fitness and adapt to selective pressures.
  • APC/C modulation may represent a common resistance mechanism against cancer therapeutics that induce chromosome segregation errors.