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

7.8K
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...
7.8K
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

4.9K
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...
4.9K
M-Cdk Drives Transition Into Mitosis02:15

M-Cdk Drives Transition Into Mitosis

5.7K
Checkpoints throughout the cell cycle serve as safeguards and gatekeepers, allowing the cell cycle to progress in favorable conditions and slow or halt it in problematic ones. This regulation is known as the cell cycle control system.
Cyclin-dependent kinases, or Cdks, work in concert with cyclins to control cell cycle transitions. M-Cdk, a complex of Cdk1 bound to M cyclin, is a well-known example of this coordinated control that drives the transition from the G2 to the M phase.
M cyclin...
5.7K

You might also read

Related Articles

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

Sort by
Same author

Trends in psychotropic use among older adults with dementia in Korean long-term care hospitals across the COVID-19 pandemic: a national longitudinal study.

Frontiers in public health·2026
Same author

Erratum to "'Site-specific enrichment of highly sialylated N-glycans in an erythropoietin-hybrid Fc fusion protein" [Eur. J. Pharm. Biopharm. 226 (2026) 115147].

European journal of pharmaceutics and biopharmaceutics : official journal of Arbeitsgemeinschaft fur Pharmazeutische Verfahrenstechnik e.V·2026
Same author

Limited Cross-Neutralization of Emerging SARS-CoV-2 BA.3.2.2 After LP.8.1-Updated Vaccination.

Journal of medical virology·2026
Same author

Differential Wound Healing Potential of Tonsil Parenchymal and Epithelial Mesenchymal Stromal Cell-Derived Exosomes.

Tissue engineering and regenerative medicine·2026
Same author

Site-specific enrichment of highly sialylated N-glycans in an erythropoietin-hybrid Fc fusion protein.

European journal of pharmaceutics and biopharmaceutics : official journal of Arbeitsgemeinschaft fur Pharmazeutische Verfahrenstechnik e.V·2026
Same author

Clinical outcomes associated with Korean medicine home-visit care for patients with cognitive impairment: a multi-center retrospective observational study.

Scientific reports·2026
Same journal

RETRACTED: Meligy et al. Therapeutic Potential of Mesenchymal Stem Cells Versus Omega n - 3 Polyunsaturated Fatty Acids on Gentamicin-Induced Cardiac Degeneration. <i>Pharmaceutics</i> 2022, <i>14</i>, 1322.

Pharmaceutics·2026
Same journal

Correction: Mohite et al. Bioactive Compound-Fortified Nanomedicine in the Modulation of Reactive Oxygen Species and Enhancement of the Wound Healing Process: A Review. <i>Pharmaceutics</i> 2025, <i>17</i>, 855.

Pharmaceutics·2026
Same journal

Metal Nanoparticle-Reinforced Hydrogels Applied in the Inhibition of Clinical Pathogens: Structural Features, Mechanisms, and Biomedical Prospects.

Pharmaceutics·2026
Same journal

Development and Evaluation of a Physiologically Based Pharmacokinetic Model for Cipepofol Across Diverse Clinical Populations.

Pharmaceutics·2026
Same journal

Artificial Intelligence in Nanopharmaceutical Development: From Predictive Design to Clinical Translation.

Pharmaceutics·2026
Same journal

Textilinin-1, a Snake Venom-Derived Kunitz-Type Protease Inhibitor, Accelerates Wound Healing Through Anti-Inflammatory, Antibacterial, and Pro-Regenerative Activities.

Pharmaceutics·2026
See all related articles

Related Experiment Video

Updated: Sep 9, 2025

High-Throughput Cellular Profiling of Targeted Protein Degradation Compounds Using HiBiT CRISPR Cell Lines
05:33

High-Throughput Cellular Profiling of Targeted Protein Degradation Compounds Using HiBiT CRISPR Cell Lines

Published on: November 9, 2020

10.1K

N-Degron-Based PROTAC Targeting PLK1: A Potential Therapeutic Strategy for Cervical Cancer.

Pethaiah Gunasekaran1,2, Sang Chul Shin3, Yeon Sil Hwang2

  • 1Division of Magnetic Resonance, Korea Basic Science Institute (KBSI), Ochang, Cheongju 28119, Republic of Korea.

Pharmaceutics
|August 28, 2025
PubMed
Summary
This summary is machine-generated.

A novel PROTAC molecule, NC1, effectively degrades Polo-like kinase 1 (PLK1) in cervical cancer cells, showing promise for overcoming chemoresistance and inhibiting tumor growth in preclinical models.

Keywords:
N-degronN-end rule pathwayPLK1PROTACanticancer

More Related Videos

Chemical Inactivation of the E3 Ubiquitin Ligase Cereblon by Pomalidomide-based Homo-PROTACs
10:44

Chemical Inactivation of the E3 Ubiquitin Ligase Cereblon by Pomalidomide-based Homo-PROTACs

Published on: May 15, 2019

13.3K
Development of Inhibitors of Protein-protein Interactions through REPLACE: Application to the Design and Development Non-ATP Competitive CDK Inhibitors
10:33

Development of Inhibitors of Protein-protein Interactions through REPLACE: Application to the Design and Development Non-ATP Competitive CDK Inhibitors

Published on: October 26, 2015

11.4K

Related Experiment Videos

Last Updated: Sep 9, 2025

High-Throughput Cellular Profiling of Targeted Protein Degradation Compounds Using HiBiT CRISPR Cell Lines
05:33

High-Throughput Cellular Profiling of Targeted Protein Degradation Compounds Using HiBiT CRISPR Cell Lines

Published on: November 9, 2020

10.1K
Chemical Inactivation of the E3 Ubiquitin Ligase Cereblon by Pomalidomide-based Homo-PROTACs
10:44

Chemical Inactivation of the E3 Ubiquitin Ligase Cereblon by Pomalidomide-based Homo-PROTACs

Published on: May 15, 2019

13.3K
Development of Inhibitors of Protein-protein Interactions through REPLACE: Application to the Design and Development Non-ATP Competitive CDK Inhibitors
10:33

Development of Inhibitors of Protein-protein Interactions through REPLACE: Application to the Design and Development Non-ATP Competitive CDK Inhibitors

Published on: October 26, 2015

11.4K

Area of Science:

  • Oncology
  • Molecular Biology
  • Drug Discovery

Background:

  • Cervical cancer presents a significant global health challenge.
  • Current chemotherapy options are limited by resistance, necessitating novel therapeutic strategies.
  • Polo-like kinase 1 (PLK1) is overexpressed in cervical cancer and represents a potential therapeutic target.

Purpose of the Study:

  • To develop a novel Proteolysis-Targeting Chimera (PROTAC) molecule targeting PLK1.
  • To investigate the efficacy of this PROTAC in degrading PLK1 and its impact on cervical cancer cells.
  • To evaluate the therapeutic potential of the PROTAC in preclinical models.

Main Methods:

  • Development of a novel PROTAC, NC1, designed to target the PLK1 protein via the N-end rule pathway.
  • Assessment of PLK1 protein depletion in HeLa cells.
  • Structural analysis of the PBD-NC1 complex and binding affinity determination using Isothermal Titration Calorimetry (ITC).
  • In vitro evaluation of cell viability, cell cycle arrest, and apoptosis induction.
  • In vivo assessment of tumor growth suppression in a HeLa xenograft mouse model.

Main Results:

  • The PROTAC NC1 successfully induced degradation of PLK1 protein in HeLa cells.
  • Structural studies confirmed key binding interactions between NC1 and PLK1 PBD, with an ITC-determined binding affinity of 6.06 µM.
  • NC1 demonstrated significant anti-cancer effects in vitro, including reduced cell viability (IC50 of 5.23 µM), G2/M phase arrest, and apoptosis induction.
  • In vivo studies showed that NC1 suppressed tumor growth in a mouse model.

Conclusions:

  • N-degron-based PROTACs targeting PLK1 are a promising strategy for cancer therapy.
  • The developed PROTAC, NC1, shows significant potential for overcoming chemoresistance in cervical cancer.
  • This research supports the development of novel PLK1-targeting PROTACs for future cervical cancer treatment strategies.