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

Intracellular Signaling Affects Focal Adhesions01:17

Intracellular Signaling Affects Focal Adhesions

2.9K
Integrins act both as extracellular input receivers and as intracellular processing activators. As their name suggests, integrins are entirely integrated into the membrane structure. Their hydrophobic membrane-spanning regions interact with the phospholipid bilayer's hydrophobic region. These membrane receptors provide extracellular attachment sites for effectors like hormones and growth factors. They activate intracellular response cascades when their effectors are bound and active.
Some...
2.9K
Metastasis02:30

Metastasis

5.7K
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...
5.7K
Cancer Cell Migration through Invadopodia01:35

Cancer Cell Migration through Invadopodia

2.4K
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,...
2.4K
Activation of Integrins01:15

Activation of Integrins

3.7K
Integrins bind ligands and transmit information from outside the cell to inside or vice-versa through an "outside-in signaling" or "inside-out signaling."
In "outside-in signaling," external factors in the extracellular space bind to exposed ligand binding sites on integrins. This causes the inactive protein to undergo a conformational change to become active. Integrins are often clustered on the cell membrane. Repetitive and regularly spaced ligand binding...
3.7K
Integrins01:10

Integrins

4.2K
Animal and protozoan cells do not have cell walls to help maintain shape and provide structural stability. Instead, these eukaryotic cells secrete a sticky mass of carbohydrates and proteins into the spaces between adjacent cells. This network of proteins and molecules is called an extracellular matrix or ECM.
Some ECM proteins assemble into a basement membrane to which the remaining components adhere. Proteoglycans typically form the bulk of the ECM while fibrous proteins, like collagen,...
4.2K
The Ras Gene02:38

The Ras Gene

6.5K
The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
Ras is a...
6.5K

You might also read

Related Articles

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

Sort by
Same author

A Clinically Integrated Pediatric Patient-Derived Xenograft Program Enables Evaluation of Cohort and Patient-Specific Biology and Therapeutic Strategies.

Cancer research·2026
Same author

Clinicogenomic analysis of <i>EGFR</i>-mutant lung tumors identifies Rb pathway inactivation as a hallmark of squamous transformation.

Science translational medicine·2026
Same author

Hierarchical classification of immune cell transcriptomes at population-scale.

bioRxiv : the preprint server for biology·2026
Same author

Impact of Dedicated Care Coordination on Access to Multidimensional Support Services in Young-Onset Colorectal Cancer: A Pragmatic Trial.

JCO oncology practice·2026
Same author

An appendiceal cancer organoid biobank identifies phenotypic evolution and druggable dependencies of peritoneal carcinomatosis.

Developmental cell·2026
Same author

Development of CAR T cells Targeting a Surface RNA Binding Protein for the Treatment of Acute Leukemias.

Cancer discovery·2026

Related Experiment Video

Updated: Sep 27, 2025

Real-Time Quantitative Measurement of Tumor Cell Migration and Invasion Following Synthetic mRNA Transfection
11:00

Real-Time Quantitative Measurement of Tumor Cell Migration and Invasion Following Synthetic mRNA Transfection

Published on: June 23, 2023

1.3K

KRAS Mutants Upregulate Integrin β4 to Promote Invasion and Metastasis in Colorectal Cancer.

Seo-Hyun Choi1, Jin K Kim1, Chin-Tung Chen1

  • 1Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, New York.

Molecular Cancer Research : MCR
|April 8, 2022
PubMed
Summary

KRAS mutations in colorectal cancer drive aggressive tumors by upregulating integrin α6β4. Targeting this protein reduces cancer cell invasion and lung metastasis, offering a potential therapeutic strategy.

More Related Videos

Impedance-based Real-time Measurement of Cancer Cell Migration and Invasion
09:23

Impedance-based Real-time Measurement of Cancer Cell Migration and Invasion

Published on: April 2, 2020

6.6K
Molecular Profiling of the Invasive Tumor Microenvironment in a 3-Dimensional Model of Colorectal Cancer Cells and Ex vivo Fibroblasts
10:33

Molecular Profiling of the Invasive Tumor Microenvironment in a 3-Dimensional Model of Colorectal Cancer Cells and Ex vivo Fibroblasts

Published on: April 29, 2014

11.2K

Related Experiment Videos

Last Updated: Sep 27, 2025

Real-Time Quantitative Measurement of Tumor Cell Migration and Invasion Following Synthetic mRNA Transfection
11:00

Real-Time Quantitative Measurement of Tumor Cell Migration and Invasion Following Synthetic mRNA Transfection

Published on: June 23, 2023

1.3K
Impedance-based Real-time Measurement of Cancer Cell Migration and Invasion
09:23

Impedance-based Real-time Measurement of Cancer Cell Migration and Invasion

Published on: April 2, 2020

6.6K
Molecular Profiling of the Invasive Tumor Microenvironment in a 3-Dimensional Model of Colorectal Cancer Cells and Ex vivo Fibroblasts
10:33

Molecular Profiling of the Invasive Tumor Microenvironment in a 3-Dimensional Model of Colorectal Cancer Cells and Ex vivo Fibroblasts

Published on: April 29, 2014

11.2K

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Metastasis

Background:

  • KRAS mutations in colorectal cancer correlate with increased tumor aggressiveness, invasiveness, and lung metastasis.
  • The precise biological mechanisms driving these aggressive phenotypes remain incompletely understood.

Purpose of the Study:

  • To investigate the role of integrin α6β4 in KRAS-mutant colorectal cancer's invasive and metastatic properties.
  • To explore the potential of targeting integrin α6β4 as a therapeutic strategy.

Main Methods:

  • Investigated the upregulation of integrin α6β4 in KRAS-mutant colorectal cancer cells via ERK/MEK signaling.
  • Utilized CRISPR-Cas9 to knock out integrin β4 (ITGB4) in KRAS-mutant colorectal cancer cells.
  • Assessed the impact of ITGB4 knockout on cancer cell invasion, migration, and pulmonary metastasis in mouse models.

Main Results:

  • KRAS-mutant colorectal cancer upregulates integrin α6β4 expression through ERK/MEK signaling.
  • ITGB4 knockout significantly reduced the invasion and migration of cancer cells.
  • Mice injected with ITGB4 knockout cells showed decreased lung metastatic foci compared to controls, with no significant difference in liver metastases.

Conclusions:

  • Integrin α6β4 is a key mediator of KRAS-mutant colorectal cancer aggressiveness and pulmonary metastasis.
  • Inhibiting integrin α6β4 presents a promising therapeutic avenue to counteract the invasive phenotype and reduce lung metastasis in KRAS-mutant colorectal cancer.