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

Metastasis02:30

Metastasis

Metastasis is the spread of cancer cells from the original site to distant locations in the body. Cancer cells can spread via blood vessels (hematogenous) as well as lymph vessels in the body.
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
Cancer Cell Migration through Invadopodia01:35

Cancer Cell Migration through Invadopodia

Invadosome is a broad category of cell surface structures with proteolytic activity that  degrades the extracellular matrix (ECM). Invadosomes are present in normal cell types, including macrophages, endothelial cells, and neurons, as well as tumor cells. Although the macrophage podosomes and tumor cell invadopodia are classified as invadosomes, they have different structures, molecular pathways, and functions. Podosomes are short structures that last for a few minutes. However, invadopodia can...

You might also read

Related Articles

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

Sort by
Same author

eIF3e-mediated translational checkpoint maintains immune tolerance and prevents lymphoid malignancy.

The Journal of experimental medicine·2026
Same author

eIF3 musketeers: loyal in health, rogue in disease, and redeemed by therapeutic targeting.

The EMBO journal·2026
Same author

Automation workflow for high-throughput arrayed plasmid DNA preparation and quantification.

bioRxiv : the preprint server for biology·2025
Same author

5' UTR-mediated retention of eIF3 on 80S ribosomes promotes co-translational folding of ER membrane proteins.

Cell reports·2025
Same author

Automation of high-throughput workflow for arrayed CRISPR activation library screening.

bioRxiv : the preprint server for biology·2025
Same author

Automation of high-throughput arrayed lentivirus production and titration.

bioRxiv : the preprint server for biology·2025

Related Experiment Video

Updated: Jun 23, 2026

Combined Use of Tail Vein Metastasis Assays and Real-Time In Vivo Imaging to Quantify Breast Cancer Metastatic Colonization and Burden in the Lungs
10:32

Combined Use of Tail Vein Metastasis Assays and Real-Time In Vivo Imaging to Quantify Breast Cancer Metastatic Colonization and Burden in the Lungs

Published on: December 19, 2019

Inflamed snail speeds metastasis.

Chih-Cheng Yang1, Dieter A Wolf

  • 1Signal Transduction Program, Burnham Institute for Medical Research, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA.

Cancer Cell
|May 5, 2009
PubMed
Summary

Tumor-promoting inflammation involves macrophages and cytokines. This study reveals how TNFalpha-NFkappaB signaling stabilizes Snail, driving cancer cell migration and metastasis.

Area of Science:

  • Oncology
  • Cell Biology
  • Molecular Biology

Background:

  • Macrophage infiltration and inflammatory cytokines are key drivers of cancer development and spread.
  • Understanding the molecular mechanisms linking inflammation to metastasis is crucial for therapeutic development.

Purpose of the Study:

  • To elucidate the molecular pathway through which inflammatory signals promote cancer cell migration and metastasis.
  • To identify key protein interactions and regulatory events involved in tumor progression.

Main Methods:

  • Investigated the role of tumor necrosis factor-alpha (TNFalpha) and nuclear factor-kappa B (NFkappaB) signaling.
  • Utilized biochemical assays to study the inhibition of glycogen synthase kinase 3 beta (GSK3beta) and SCF(beta-TRCP) ubiquitin ligase.
  • Analyzed the stabilization of the transcription factor Snail and its impact on cell migration.

More Related Videos

Experimental Metastasis Assay
08:28

Experimental Metastasis Assay

Published on: August 24, 2010

CAM-Delam Assay to Score Metastatic Properties by Quantifying Delamination and Invasion Capacity of Cancer Cells
12:14

CAM-Delam Assay to Score Metastatic Properties by Quantifying Delamination and Invasion Capacity of Cancer Cells

Published on: June 2, 2022

Related Experiment Videos

Last Updated: Jun 23, 2026

Combined Use of Tail Vein Metastasis Assays and Real-Time In Vivo Imaging to Quantify Breast Cancer Metastatic Colonization and Burden in the Lungs
10:32

Combined Use of Tail Vein Metastasis Assays and Real-Time In Vivo Imaging to Quantify Breast Cancer Metastatic Colonization and Burden in the Lungs

Published on: December 19, 2019

Experimental Metastasis Assay
08:28

Experimental Metastasis Assay

Published on: August 24, 2010

CAM-Delam Assay to Score Metastatic Properties by Quantifying Delamination and Invasion Capacity of Cancer Cells
12:14

CAM-Delam Assay to Score Metastatic Properties by Quantifying Delamination and Invasion Capacity of Cancer Cells

Published on: June 2, 2022

Main Results:

  • Demonstrated that TNFalpha-dependent NFkappaB activation leads to COP9 signalosome-mediated inhibition of GSK3beta.
  • Showed that this inhibition prevents the ubiquitylation and degradation of the transcription factor Snail by the SCF(beta-TRCP) ubiquitin ligase.
  • Confirmed that Snail stabilization promotes cancer cell migration and metastasis.

Conclusions:

  • The inflammatory pathway involving TNFalpha and NFkappaB plays a critical role in promoting cancer metastasis through Snail stabilization.
  • Targeting this pathway could offer novel therapeutic strategies to inhibit tumor cell migration and prevent metastasis.