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

Nondisjunction01:21

Nondisjunction

3.9K
Nondisjunction is the failure of homologous chromosomes or sister chromatids to separate correctly and move to the opposite poles of the cells. This produces daughter cells with abnormal chromosome numbers.  Nondisjunction is common during anaphase I or anaphase II of meiosis.  Mutations in synaptonemal complex proteins that attach homologous chromosomes increase the chances of nondisjunction in anaphase I of meiosis I. In contrast, mutations in topoisomerases and condensins that hold...
3.9K
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

4.8K
The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
4.8K

You might also read

Related Articles

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

Sort by
Same author

Deep-learning-enabled multi-omics analyses for prediction of future metastasis in cancer.

bioRxiv : the preprint server for biology·2025
Same author

The Kinesin-14 tail: Dual microtubule binding domains drive spindle morphogenesis through tight microtubule cross-linking and robust sliding.

Molecular biology of the cell·2025
Same author

Amyloidogenesis promotes HSF1 activity enhancing cell survival during breast cancer metastatic colonization.

Cell stress & chaperones·2025
Same author

SUV39H1 maintains cancer stem cell chromatin state and properties in glioblastoma.

JCI insight·2025
Same author

The Kinesin-14 Tail: Dual microtubule binding domains drive spindle morphogenesis through tight microtubule cross-linking and robust sliding.

bioRxiv : the preprint server for biology·2025
Same author

MYC and HSF1 Cooperate to Drive Sensitivity to Polo-like Kinase 1 Inhibitor Volasertib in High-grade Serous Ovarian Cancer.

Cancer research communications·2025

Related Experiment Video

Updated: Jul 23, 2025

Studying Triple Negative Breast Cancer Using Orthotopic Breast Cancer Model
09:29

Studying Triple Negative Breast Cancer Using Orthotopic Breast Cancer Model

Published on: March 20, 2020

17.8K

MCAK Inhibitors Induce Aneuploidy in Triple-Negative Breast Cancer Models.

John C Smith1, Stefan Husted2, Jay Pilrose3

  • 1Medical Sciences, Indiana School of Medicine-Bloomington, Bloomington, IN 47405, USA.

Cancers
|July 14, 2023
PubMed
Summary

Targeting MCAK, a protein that limits aneuploidy, shows promise for treating triple-negative breast cancer (TNBC). Inhibiting MCAK sensitizes TNBC cells to paclitaxel and may serve as a prognostic biomarker.

Keywords:
MCAK/KIF2Caneuploidychromosomal instabilitydrug discoverytriple-negative breast cancer

More Related Videos

Author Spotlight: Exploring the Role of FAM83A in Cervical Cancer
04:20

Author Spotlight: Exploring the Role of FAM83A in Cervical Cancer

Published on: February 9, 2024

972
A Portal Vein Injection Model to Study Liver Metastasis of Breast Cancer
07:35

A Portal Vein Injection Model to Study Liver Metastasis of Breast Cancer

Published on: December 26, 2016

41.2K

Related Experiment Videos

Last Updated: Jul 23, 2025

Studying Triple Negative Breast Cancer Using Orthotopic Breast Cancer Model
09:29

Studying Triple Negative Breast Cancer Using Orthotopic Breast Cancer Model

Published on: March 20, 2020

17.8K
Author Spotlight: Exploring the Role of FAM83A in Cervical Cancer
04:20

Author Spotlight: Exploring the Role of FAM83A in Cervical Cancer

Published on: February 9, 2024

972
A Portal Vein Injection Model to Study Liver Metastasis of Breast Cancer
07:35

A Portal Vein Injection Model to Study Liver Metastasis of Breast Cancer

Published on: December 26, 2016

41.2K

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Standard treatment for triple-negative breast cancer (TNBC) uses paclitaxel, a microtubule poison that induces aneuploidy.
  • While initially effective, paclitaxel treatment often leads to dose-limiting peripheral neuropathies and the development of drug-resistant tumors.
  • Identifying novel therapeutic targets is crucial for overcoming resistance and improving TNBC treatment outcomes.

Purpose of the Study:

  • To investigate the role of the microtubule depolymerizing kinesin, MCAK, as a potential therapeutic target in TNBC.
  • To determine if MCAK inhibition can sensitize TNBC cells to paclitaxel and overcome drug resistance.
  • To evaluate MCAK as a prognostic biomarker in TNBC.

Main Methods:

  • Analysis of publicly available datasets to assess MCAK expression and its correlation with prognosis in TNBC.
  • In vitro knockdown of MCAK in TNBC cell lines to evaluate its effect on paclitaxel sensitivity.
  • High-throughput screening of a compound library to identify MCAK inhibitors using FRET and image-based assays.

Main Results:

  • MCAK is upregulated in TNBC and associated with poorer patient prognoses.
  • MCAK knockdown significantly reduced paclitaxel IC50 in TNBC cells without affecting normal cells.
  • Three novel MCAK inhibitors were identified, which induced aneuploidy, reduced TNBC cell survival, and sensitized cells to paclitaxel.

Conclusions:

  • MCAK is a promising therapeutic target for TNBC, potentially overcoming paclitaxel resistance.
  • MCAK inhibition represents a viable strategy to enhance the efficacy of existing chemotherapies.
  • MCAK may serve as a valuable prognostic biomarker for triple-negative breast cancer.